Updated on 2023/11/30

写真a

 
SUZUKI, Hiromi
 
Organization
Research Institute of Environmental Medicine Division of Stress Adaptation and Protection Assistant Professor
Graduate School
Graduate School of Medicine
Title
Assistant Professor
Contact information
メールアドレス
External link

Degree 2

  1. 医学博士 ( 2003.3   藤田保健衛生大学 ) 

  2. 衛生学士 ( 1990.3   藤田保健衛生大学 ) 

Research Interests 3

  1. Imaging

  2. DDS

  3. microglia

Research Areas 1

  1. Others / Others  / 神経化学 神経病理学

Current Research Project and SDGs 9

  1. LMD-LC-MSによる脳内の薬物動態と神経伝達物質変化の細胞毎イメージング

  2. ミクログリア機能を反映するPETイメージング

  3. MALDI MSイメージングでの生体高分子の検出やLC-MS/MS分析でも質量イメージングを可能にする技術の確立

  4. 脳特異的ドラッグデリバリシステムの構築、微小血管解析システムを用いた脳・神経系ヘの細胞浸潤のイメージング

  5. 脳標的化ペプチドを用いた脳疾患のPET診断用システム開発

  6. 脳病態における活性化ミクログリアの毒性転換のメカニズム

  7. 脳標的化分子の単離

  8. 脳イメージングのためのリガンド輸送ツール開発

  9. 脳への選択的物質輸送システムの開発

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Research History 20

  1. Nagoya University   Graduate School of Medicine   Assistant Professor

    2022.1

  2. Nagoya University   Assistant Professor

    2009.3

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    Country:Japan

  3. 株式会社ティッシュターゲティングジャパン    研究開発部   主任研究員

    2005.3 - 2009.2

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    Country:Japan

  4. OTAGO univ.   Department of Physiology   Researcher

    2003.5 - 2003.6

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    Country:New Zealand

  5. 藤田保健衛生大学(藤田医科大学)   放射線科   客員助教

    2019.4

  6. Nagoya University   Research Institute of Environmental Medicine Division of Stress Adaptation and Protection   Assistant Professor

    2009.3

  7. 株式会社ティッシュターゲティングジャパン 研究開発部 主任研究員

    2005.3 - 2009.2

  8. Department of Physiology, OTAGO univ.

    2003.5 - 2003.6

  9. 放射線医学総合研究所    研究員

    2003.4 - 2012.3

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    Country:Japan

  10. 放射線医学総合研究所 客員協力研究員

    2003.4 - 2012.3

  11. Nagoya University   Researcher

    2003.4 - 2009.2

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    Country:Japan

  12. 名古屋大学環境医学研究所 脳機能分野 客員研究者

    2003.4 - 2009.2

  13. Fujita Health University   Assistant

    2003.4 - 2005.2

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    Country:Japan

  14. 藤田保健衛生大学総合医科学研究所 難病治療共同研究部門 助手

    2003.4 - 2005.2

  15. 科学技術振興事業団さきがけ    研究員

    2001.9 - 2002.2

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    Country:Japan

  16. 科学技術振興事業団さきがけ 研究補助員

    2001.9 - 2002.2

  17. Fujita Health University   Researcher

    2001.4 - 2003.3

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    Country:Japan

  18. 藤田保健衛生大学総合医科学研究所難病治療共同研究部門 研究員

    2001.4 - 2003.3

  19. 藤田学園保健衛生大学医学部脳神経外科 研究員

    1994.4 - 2001.3

  20. Fujita Health University   Researcher

    1990.4 - 2001.3

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    Country:Japan

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Education 2

  1. Fujita Health University

    - 2003.3

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    Country: Japan

  2. Fujita Health University

    1986.4 - 1990.3

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    Country: Japan

Professional Memberships 4

  1. 日本分子イメージング学会

  2. 日本バイオイメージング学会

  3. 日本神経化学会

  4. The Molecular Biology Society of Japan

 

Papers 82

  1. LC-MS/MS imaging with thermal film-based laser microdissection Reviewed International coauthorship International journal

    Michiko Oya, Hiromi Suzuki, Andrea Roxanne J. Anas, Koichi Oishi, Kenji Ono, Shun Yamaguchi, Megumi Eguchi, Makoto Sawada

    Analytical and Bioanalytical Chemistry   Vol. 410 ( 2 ) page: 491 - 499   2018.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Verlag  

    Mass spectrometry (MS) imaging is a useful tool for direct and simultaneous visualization of specific molecules. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is used to evaluate the abundance of molecules in tissues using sample homogenates. To date, however, LC-MS/MS has not been utilized as an imaging tool because spatial information is lost during sample preparation. Here we report a new approach for LC-MS/MS imaging using a thermal film-based laser microdissection (LMD) technique. To isolate tissue spots, our LMD system uses a 808-nm near infrared laser, the diameter of which can be freely changed from 2.7 to 500 μm
    for imaging purposes in this study, the diameter was fixed at 40 μm, allowing acquisition of LC-MS/MS images at a 40-μm resolution. The isolated spots are arranged on a thermal film at 4.5-mm intervals, corresponding to the well spacing on a 384-well plate. Each tissue spot is handled on the film in such a manner as to maintain its spatial information, allowing it to be extracted separately in its individual well. Using analytical LC-MS/MS in combination with the spatial information of each sample, we can reconstruct LC-MS/MS images. With this imaging technique, we successfully obtained the distributions of pilocarpine, glutamate, γ-aminobutyric acid, acetylcholine, and choline in a cross-section of mouse hippocampus. The protocol we established in this study is applicable to revealing the neurochemistry of pilocarpine model of epilepsy. Our system has a wide range of uses in fields such as biology, pharmacology, pathology, and neuroscience. [Figure not available: see fulltext.].

    DOI: 10.1007/s00216-017-0739-2

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  2. Signal Sequence-Dependent Orientation of Signal Peptide Fragments to Exosomes. Reviewed

    Ono K, Niwa M, Suzuki H, Kobayashi NB, Yoshida T, Sawada M

    International Journal of Molecular Sciences   Vol. 23 ( 6 ) page: 3137   2022.3

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    Signal peptides (SPs) not only mediate targeting to the endoplasmic reticulum (ER) but also play important roles as biomarkers and substances with physiological activity in extracellular fluids including blood. SPs are thought to be degraded intracellularly, making it unclear how they are transported from the ER to the extracellular fluid. In a recent study, we showed that a C-terminal fragment of the SP of a type I membrane protein, amyloid precursor protein (APP), was secreted into the extracellular fluid via exosomes using transformed HEK293 cells expressing APP SP flanking a reporter protein. In the present study, we demonstrate that a N-terminal fragment of the SP from a type II membrane protein, human placental secreted alkaline phosphatase (SEAP), is contained in exosomes and secreted into the extracellular fluid using HEK-Blue hTLR3 cells, which express both a human toll-like receptor 3 gene and an inducible SEAP reporter gene. When HEK-Blue hTLR3 cells were stimulated with a TLR3 ligand, a N-terminal fragment of SEAP SP in exosomes was increased in parallel with SEAP secretion in a concentration-dependent manner. These results indicated that SP fragments are exosomal components. In addition, migrating SP fragments were determined by characteristics of the signal–anchor sequence of membrane proteins. Furthermore, we found that SP fragments could bind to calmodulin (CALM), which is a cytosolic protein and also a component of exosomes, suggesting its involvement in the transportation of SP fragments from the endoplasmic reticulum to exosomes.

    DOI: 10.3390/ijms23063137

    Other Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8950404/

  3. Secretion of signal peptides via extracellular vesicles Reviewed International journal

    Ono K, Niwa M, Suzuki H, Kobayashi NB, Yoshida T, Sawada M.

    Biochem Biophys Res Commun .   Vol. 560   page: 21 - 26   2021.5

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Elsevier  

    Signal peptides (SPs) consist of short peptide sequences present at the N-terminal of newly synthesizing proteins and act as a zip code for the translocation of the proteins to the endoplasmic reticulum (ER). It was thought that the SPs are intracellularly degraded after translocation to the ER; however, recent studies showed cleaved SPs have diverse roles for controlling cell functions in auto- and/or intercellular manners. In addition, it still remains obscure how SP fragments translocate away from the site where they are produced. Extracellular vesicles (EV) are important for intercellular communication and can transport functional molecules to specific cells. In this study, we show that SPs are involved in EV from T-REx AspALP cells that were transfected with a human APP SP-inducible expression vector. There was no difference in the average particle size or particle concentration of EV collected from T-REx AspALP cells and T-REx Mock cells. When the SP content in the EV was examined by mass spectrometry, the C-terminal fragment of APP SP was identified in the exosomes (SEV) of T-REx AspALP cells. In our preparation of SEV fractions, no ER-specific proteins were detected; therefore, SPs may be included in SEV but not in the debris of degraded ER. This is the first indication that SPs are secreted from cells via EV.

    DOI: 10.1016/j.bbrc.2021.04.073.

  4. Peripheral benzodiazepine receptor/18 kDa translocator protein positron emission tomography imaging in a rat model of acute brain injury Reviewed International coauthorship

    Nomura M, Toyama H, Suzuki H, Yamada T, Hatano K, Alan A Wilson, Ito K, Sawada M

    Ann Null Med.   Vol. 35 ( 1 ) page: 8 - 16   2021.1

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    DOI: https://doi.org/10.1007/s12149-020-01530-2

  5. Distribution of Signal Peptides in Microvesicles from Activated Macrophage Cells Invited Reviewed

    International Journal of Molecular Science   Vol. 24 ( 15 )   2023.7

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.3390/ijms241512131

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  6. Calmodulin as a Key Regulator of Exosomal Signal Peptides. Invited Reviewed International journal

    Kenji Ono, Mikio Niwa, Hiromi Suzuki, Nahoko Bailey Kobayashi, Tetsuhiko Yoshida, Makoto Sawada

    Cells   Vol. 12 ( 1 ) page: 158   2022.12

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    Signal peptides (SPs) and their fragments play important roles as biomarkers and substances with physiological functions in extracellular fluid. We previously reported that SP fragments were released into extracellular fluid via exosomes and bound to calmodulin (CaM), an exosomal component, in a cell-free system. However, it currently remains unclear whether CaM intracellularly interacts with SP fragments or is involved in the trafficking of these fragments to exosomes. Therefore, the present study examined the binding of CaM to SP fragments in T-REx AspALP cells, transformed HEK293 cells expressing amyloid precursor protein (APP) SP flanking a reporter protein, and their exosomes. APP SP fragments were detected in exosomes from T-REx AspALP cells in the absence of W13, a CaM inhibitor, but were present in lower amounts in exosomes from W13-treated cells. Cargo proteins, such as Alix, CD63, and CD81, were increased in W13-treated T-REx AspALP cells but were decreased in their exosomes. Furthermore, CaM interacted with heat shock protein 70 and CD81 in T-REx AspALP cells and this increased in the presence of W13. APP SP fragments were detected in intracellular CaM complexes in the absence of W13, but not in its presence. These results indicate that CaM functions as a key regulator of the transport of SP fragments into exosomes and plays novel roles in the sorting of contents during exosomal biogenesis.

    DOI: 10.3390/cells12010158

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  7. Inhibition of cellular inflammatory mediator production and amelioration of learning deficit in flies by deep sea Aspergillus-derived cyclopenin. Reviewed International coauthorship

    Wang L, Li M, Lin Y, Du S, Liu Z, Ju J, Suzuki H, Sawada M, Umezawa K

    The Journal of antibiotics   Vol. 73 ( 9 ) page: 622 - 629   2020.9

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    In the course of screening lipopolysaccharide (LPS)-induced nitric oxide (NO) production inhibitors, two related benzodiazepine derivatives, cyclopenol and cyclopenin, were isolated from the extract of a deep marine-derived fungal strain, Aspergillus sp. SCSIOW2. Cyclopenol and cyclopenin inhibited the LPS-induced formation of NO and secretion of IL-6 in RAW264.7 cells at nontoxic concentrations. In terms of the mechanism underlying these effects, cyclopenol and cyclopenin were found to inhibit the upstream signal of NF-κB activation. These compounds also inhibited the expression of IL-1β, IL-6, and inducible nitric oxide synthase (iNOS) in mouse microglia cells, macrophages in the brain. In relation to the cause of Alzheimer’s disease, amyloid-β-peptide is known to induce inflammation in the brain. Therefore, the present study investigated the ameliorative effects of these inhibitors on an in vivo Alzheimer’s model using flies. Learning deficits were induced by the overexpression of amyloid-β42 in flies, and cyclopenin but not cyclopenol was found to rescue learning impairment. Therefore, novel anti-inflammatory activities of cyclopenin were identified, which may be useful as a candidate of anti-inflammatory agents for neurodegenerative diseases.

    DOI: 10.1038/s41429-020-0302-9

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  8. Dipeptidyl peptidase-4 inhibition prevents nonalcoholic steatohepatitis-associated liver fibrosis and tumor development in mice independently of its anti-diabetic effects Reviewed International coauthorship

    Mitsuhiro Kawakubo, Miyako Tanaka, Kozue Ochi, Akiko Watanabe, Marie Saka-Tanaka, Yohei Kanamori, Naoki Yoshioka, Satoko Yamashita, Moritaka Goto, Michiko Itoh, Ibuki Shirakawa, Sayaka Kanai, Hiromi Suzuki, Makoto Sawada, Ayaka Ito, Masatoshi Ishigami, Mitsuhiro Fujishiro, Hiroshi Arima, Yoshihiro Ogawa, Takayoshi Suganami

    Science Report   Vol. 10 ( 1 ) page: 983   2020.1

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    Nonalcoholic steatohepatitis (NASH) is a hepatic phenotype of the metabolic syndrome, and increases the risk of cirrhosis and hepatocellular carcinoma (HCC). Although increasing evidence points to the therapeutic implications of certain types of anti-diabetic agents in NASH, it remains to be elucidated whether their effects on NASH are independent of their effects on diabetes. Genetically obese melanocortin 4 receptor-deficient (MC4R-KO) mice fed Western diet are a murine model that sequentially develops hepatic steatosis, NASH, and HCC in the presence of obesity and insulin resistance. In this study, we investigated the effect of the dipeptidyl peptidase-4 (DPP-4) inhibitor anagliptin on NASH and HCC development in MC4R-KO mice. Anagliptin treatment effectively prevented inflammation, fibrosis, and carcinogenesis in the liver of MC4R-KO mice. Interestingly, anagliptin only marginally affected body weight, systemic glucose and lipid metabolism, and hepatic steatosis. Histological data and gene expression analysis suggest that anagliptin treatment targets macrophage activation in the liver during the progression from simple steatosis to NASH. As a molecular mechanism underlying anagliptin action, we showed that glucagon-like peptide-1 suppressed proinflammatory and profibrotic phenotypes of macrophages in vitro. This study highlights the glucose metabolism-independent effects of anagliptin on NASH and HCC development.

    DOI: 10.1038/s41598-020-57935-6

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  9. Novel Oxindole-Curcumin Hybrid Compound for Antioxidative Stress and Neuroprotection Reviewed

    Yoko Hirata, Yuki Ito, Madoka Takashima, Kazuya Yagyu, Kentaro Oh-Hashi, Hiromi Suzuki, Kenji Ono, Kyoji Furuta, Makoto Sawada

    ACS Chem Neurosci .   Vol. 11 ( 1 ) page: 76-85   2020.1

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    Oxidative stress plays an important role in the pathogenesis of Parkinson's disease and other neurodegenerative disorders. The oxindole compound GIF-2165X-G1 is a hybrid molecule composed of the oxindole skeleton of the neuroprotective compound GIF-0726-r and the polyphenolic skeleton of the antioxidant curcumin. We previously reported that novel oxindole derivatives such as GIF-0726-r and GIF-2165X-G1 prevent endogenous oxidative stress-induced cell death in mouse hippocampal HT22 cells. In this study, we present a detailed investigation of the effect of GIF-2165X-G1 on endogenous oxidative stress in HT22 cells in comparison with GIF-0726-r and curcumin. GIF-2165X-G1 exhibited more potent neuroprotective activity than GIF-0726-r or curcumin and had less cytotoxicity than that observed with curcumin. Both GIF-0726-r and GIF-2165X-G1 were found to have ferrous ion chelating activity similar to that exhibited by curcumin. GIF-2165 X-G1 and curcumin induced comparable antioxidant response element transcriptional activity. Although the induction of heme oxygenase-1, an antioxidant response element-regulated gene product, was much stronger in curcumin-treated cells than in GIF-2165X-G1-treated cells, it turned out that the induction of heme oxygenase-1 is dispensable for neuroprotection. These results demonstrate that the introduction of the polyphenol skeleton of curcumin to the oxindole GIF-0726-r improves neuroprotective features. Furthermore, intrastriatal injection of GIF-2165X-G1 alleviated apomorphine-induced rotation and prevented dopaminergic neuronal loss in a 6-hydroxydopamine mouse model of Parkinson's diseases. Collectively, our novel findings indicate that the novel oxindole compound GIF-2165X-G1 serves to delay the progression of Parkinson's disease by suppressing oxidative stress.

    DOI: 10.1021/acschemneuro.9b00619.

  10. Novel oxindole derivatives prevent oxidative stress-induced cell death in mouse hippocampal HT22 cells. Reviewed

    Hirata Y, Yamada C, Ito Y, Yamamoto S, Nagase H, Oh-Hashi K, Kiuchi K, Suzuki H, Sawada M, Furuta K

    Neuropharmacology   Vol. 135   page: 242-252   2018.3

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    The current medical and surgical therapies for neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease offer symptomatic relief but do not provide a cure. Thus, small synthetic compounds that protect neuronal cells from degeneration are critically needed to prevent and treat these. Oxidative stress has been implicated in various pathophysiological conditions, including neurodegenerative diseases. In a search for neuroprotective agents against oxidative stress using the murine hippocampal HT22 cell line, we found a novel oxindole compound, GIF-0726-r, which prevented oxidative stress-induced cell death, including glutamate-induced oxytosis and erastin-induced ferroptosis. This compound also exerted a protective effect on tunicamycin-induced ER stress to a lesser extent but had no effect on campthothecin-, etoposide- or staurosporine-induced apoptosis. In addition, GIF-0726-r was also found to be effective after the occurrence of oxidative stress. GIF-0726-r was capable of inhibiting reactive oxygen species accumulation and Ca2+ influx, a presumed executor in cell death, and was capable of activating the antioxidant response element, which is a cis-acting regulatory element in promoter regions of several genes encoding phase II detoxification enzymes and antioxidant proteins. These results suggest that GIF-0726-r is a low-molecular-weight compound that prevents neuronal cell death through attenuation of oxidative stress. Among the more than 200 derivatives of the GIF-0726-r synthesized, we identified the 11 most potent activators of the antioxidant response element and characterized their neuroprotective activity in HT22 cells.

    DOI: 10.1016/j.neuropharm.2018.03.015

    PubMed

  11. Inducible nitric oxide synthase during the late phase of sepsis is associated with hypothermia and immune cell migration. Reviewed

    Takatani Y, Ono K, Suzuki H, Inaba M, Sawada M, Matsuda N

    Laboratory investigation   Vol. 98 ( 5 ) page: 629 - 639   2018.2

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    Hypothermia is a significant sign of sepsis, which is associated with poor prognosis, but few mechanisms underlying the regulation of hypothermia are known. Inducible nitric oxide synthase (iNOS) is a key inflammatory mediator of sepsis. However, the therapeutic benefit of iNOS inhibition in sepsis is still controversial, and requires elucidation in an accurate model system. In this study, wild-type (WT) mice showed temperature drops in a biphasic manner at the early and late phase of sepsis, and all mice died within 48 h of sepsis. In contrast, iNOS-knockout (KO) mice never showed the second temperature drop and exhibited improved mortality. Plasma nitric oxide (NO) levels of WT mice increased in the late phase of sepsis and correlated to hypothermia. The results indicate that iNOS-derived NO during the late phase of sepsis caused vasodilation-induced hypothermia and a lethal hypodynamic state. The expression of the iNOS mRNA was high in the lung of WT mice with sepsis, which reflects the pathology of acute respiratory distress syndrome (ARDS). We obtained the results in a modified keyhole-type cecal ligation and puncture model of septic shock induced by minimally invasive surgery. In this accurate and reproducible model system, we transplanted the bone marrow cells of GFP transgenic mice into WT and iNOS-KO mice, and evaluated the role of increased pulmonary iNOS expression in cell migration during the late phase of sepsis. We also investigated the quantity and type of bone marrow-derived cells (BMDCs) in the lung. The number of BMDCs in the lung of iNOS-KO mice was less than that in the lung of WT mice. The major BMDCs populations were CD11b-positive, iNOS-negative cells in WT mice, and Gr-1-positive cells in iNOS-KO mice that expressed iNOS. These results suggest that sustained hypothermia may be a beneficial guide for future iNOS-targeted therapy of sepsis, and that iNOS modulated the migratory efficiency and cell type of BMDCs in septic ARDS.

    DOI: 10.1038/s41374-018-0021-z

    PubMed

  12. Visualization of Arc promoter-driven neuronal activity by magnetic resonance imaging Reviewed

    Qi Wu, Kenji Ono, Hiromi Suzuki, Megumi Eguchi, Shun Yamaguchi, Makoto Sawada

    Neuroscience Letters   Vol. 666   page: 92 - 97   2018.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Elsevier Ireland Ltd  

    Visualization of direct neuronal activity to understand brain function is one of the most important challenges in neuroscience. We have previously demonstrated that in vivo and in vitro gene expression of the ferritin reporter system could be detected by magnetic resonance imaging (MRI). In addition, increased neuronal activity induces Arc, an immediate early gene, and insertion of a destabilized fluorescent reporter dVenus under Arc promoter control has been used for monitoring neuronal activities in the brain by optical imaging. In this study, to visualize Arc promoter-driven neuronal activities directly, we generated transgenic mice and cell lines that express a destabilized fusion reporter ferritin-mKate2 under Arc promoter control. When transgenic mice and cell lines were treated with pilocarpine, a non-selective muscarinic agonist, an increase in T2-weighted image signal was successfully found in neuronal cells. There was a difference in peak time between MRI and fluorescence imaging, which might result from the binding process of iron with ferritin. Visualization of Arc promoter-driven neuronal activity is essential to understand neural mechanisms underlying cognitive processes and complex behaviors, and could be a useful tool for therapeutic approaches in the brain by MRI.

    DOI: 10.1016/j.neulet.2017.12.041

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  13. Optogenetic control of cell differentiation in channelrhodopsin-2-expressing OS3, a bipotential glial progenitor cell line

    Ono K, Suzuki H, Yamamoto R, Sahashi H, Takido Y, Sawada M.

    Neurochemistry International   Vol. 104   page: 49-63   2017.3

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    DOI: 10.1016/j.neuint.2016.12.022.

  14. Radiosynthesis and in vivo evaluation of two imidazopyridineacetamides, [11C]CB184 and [ 11C]CB190, as a PET tracer for 18 kDa translocator protein: direct comparison with [ 11C](R)-PK11195. Invited Reviewed

    Hatano K, Sekimata K, Yamada T, Abe J, Ito K, Ogawa M, Magata Y, Toyohara J, Ishiwata K, Biggio G, Serra M, Laquintana V, Denora N, Latrofa A, Trapani G, Liso G, Suzuki H, Sawada M, Nomura M, Toyama H.

    Annals of nuclear medicine   Vol. 29 ( 4 ) page: 325 - 35   2015.5

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    DOI: 10.1007/s12149-015-0948-8

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  15. Protective effect of INI-0602, a gap junction inhibitor, on dopaminergic neurodegeneration of mice with unilateral 6-hydroxydopamine injection

    SUZUKI Hiromi,ONO Kenji,SAWADA Makoto

    Journal of Neural Transmission   Vol. 121 ( 11 ) page: 1349-1355   2014.11

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    DOI: 10.1007/s00702-014-1209-z.

  16. Glutamate release from astrocyte cell-line GL261 via alterations in the intracellular ion environment Reviewed

    Kenji Ono, Hiromi Suzuki, Madoka Higa, Kaori Tabata, Makoto Sawada

    JOURNAL OF NEURAL TRANSMISSION   Vol. 121 ( 3 ) page: 245 - 57   2014

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    Astrocytes modify and maintain neural activity and functions via gliotransmitter release such as, glutamate. They also change their properties and functions in response to alterations of ion environment resulting from neurotransmission; however, the direct evidence for whether intracellular ion alteration in astrocytes triggers gliotransmitter release is not indicated. Recent studies have reported that channelrhodopsin-2 (ChR2) is useful for alteration of intracellular ion environment in several types of cells with blue light exposure. Here, we show that ChR2-expressing GL261 (GLChR2) cells, clonal astrocytes, change their properties by photo-activation. Increased intracellular sodium and calcium ion concentrations and an altered membrane potential were observed in GLChR2 cells with blue light exposure. Alterations in the intracellular ion environment caused intracellular acidification and the inhibition of proliferation. In addition, it triggered glutamate release from GLChR2 cells. Glutamate from GLChR2 cells acted on N18 cells, clonal neuronal cells, as both a transmitter and neurotoxin depending on photo-activation. Our results show that the properties of ChR2-expressing astrocytes can be controlled by blue light exposure, and cation influx through photo-activated ChR2 might trigger functional cation influx via endogenous channels and result in the increase of glutamate release. Further, our results suggest that ChR2-expressing glial cells could become a useful tool in understanding the roles of glial cell activation and neural communication in the regulation of brain functions.

    DOI: 10.1007/s00702-013-1096-8

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  17. Detection of cytotoxic activation of microglia in a rat neuroinflammation model using a novel translocator protein ligand, [18F]FEPPA Invited Reviewed

    Nomura, M; Toyama, H; Suzuki, H; Yamada, T; Ota, S; Ichise, M; Wilson, A; Sawada, M; Ito, K; Hatano, K

    JOURNAL OF NUCLEAR MEDICINE   Vol. 53   2012.5

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

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  18. Detection of cytotoxic activation of microglia in a rat neuroinflammation model using a novel translocator protein ligand, [18F]FEPPA Reviewed

    Nomura,M, Toyama,H, Suzuki,H, Yamada,T, Ota,S, Ichise,M, Wilson,AA, Sawada,M, Ito,K, Hatano,K

    J Nucl Med   Vol. 53(Supplement 1)   page: 1884   2012

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  19. New fluorescent probes targeting the mitochondrial-located translocator protein 18 kDa (TSPO) as activated microglia imaging agents. Reviewed

    DENORA N, LAQUINTANA V, TRAPANI A, SUZUKI H, SAWADA M, TRAPANI G

    Pharmaceutical Research   Vol. 28 ( 11 ) page: 2820-2832   2011.11

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  20. New Fluorescent Probes Targeting the Mitochondrial-Located Translocator Protein 18 kDa (TSPO) as Activated Microglia Imaging Agents Reviewed

    Nunzio Denora, Valentino Laquintana, Adriana Trapani, Hiromi Suzuki, Makoto Sawada, Giuseppe Trapani

    PHARMACEUTICAL RESEARCH   Vol. 28 ( 11 ) page: 2820 - 2832   2011.11

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:SPRINGER/PLENUM PUBLISHERS  

    To evaluate the utility of new Translocator protein 18 kDa (TSPO)-targeted fluorescent probes for in vivo molecular imaging of activated microglia.
    Compounds 2-4 were synthesized; their stability and affinity for TSPO were determined. Compounds 2-4 were incubated both with Ra2 cells in the presence of LPS, a potent activator of microglia, and with tissue sections of normal and chemically injured brains. Compounds 2-4 were injected into carotid artery or directly in striatum of mice. Cells and tissue sections from these in vitro and in vivo studies were observed by fluorescence microscopy after histochemical treatments.
    Compounds 2-4 are stable in both buffer and physiological medium and showed high affinity for TSPO and were found to stain live Ra2 microglial cells effectively. Double staining with Mito Tracker Red suggested that binding sites of compounds 2 and 3 may exist on mitochondria. In vivo studies showed that compounds 2-4 may penetrate in part into brain; moreover, cells in mouse striatum were stained with compounds 2-4 and microglial marker CD11b.
    Compounds 2-4 can fluorescently label activated microglia in vitro and in vivo.

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  21. Time-dependent changes in proinflammatory and neurotrophic responses of microglia and astrocytes in a rat model of osmotic demyelination syndrome. Reviewed

    IWAMA S, SUGIMURA Y, SUZUKI H, SUZUKI H, MURASE T, OZAKI N, NAGASAKI H, ARIMA H, MURATA Y, SAWADA M, OISO Y

    Glia   Vol. 59 ( 3 ) page: 452-462   2011.3

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  22. Time-Dependent Changes in Proinflammatory and Neurotrophic Responses of Microglia and Astrocytes in a Rat Model of Osmotic Demyelination Syndrome Reviewed

    Shintaro Iwama, Yoshihisa Sugimura, Haruyuki Suzuki, Hiromi Suzuki, Takashi Murase, Nobuaki Ozaki, Hiroshi Nagasaki, Hiroshi Arima, Yoshiharu Murata, Makoto Sawada, Yutaka Oiso

    GLIA   Vol. 59 ( 3 ) page: 452 - 462   2011.3

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    Osmotic demyelination syndrome (ODS) is a serious demyelinating disease in the central nervous system usually caused by rapid correction of hyponatremia. In an animal model of ODS, we previously reported microglial accumulation expressing proinflammatory cytokines. Microglia and astrocytes secreting proinflammatory cytokines and neurotrophic factors are reported to be involved in the pathogenesis of demyelinative diseases. Therefore, to clarify the role of microglial and astrocytic function in ODS, we examined the time-dependent changes in distribution, morphology, proliferation, and mRNA/protein expression of proinflammatory cytokines, neurotrophic factors, and matrix metalloproteinase (MMP) in microglia and astrocytes 2 days (early phase) and 5 days (late phase) after the rapid correction of hyponatremia in ODS rats. The number of microglia time dependently increased at demyelinative lesion sites, proliferated, and expressed tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6, inducible nitric oxide synthase, and MMP2, 9, and 12 at the early phase. Microglia also expressed leukemia inhibitory factor (a neurotrophic factor) and phagocytosed myelin debris at the late phase. The number of astrocytes time dependently increased around demyelinative lesions, extended processes to lesions, proliferated, and expressed nerve growth factor and glial cell line-derived neurotrophic factor at the late phase. Moreover, treatment with infliximab, a monoclonal antibody against TNF-alpha, significantly attenuated neurological impairments. Our results suggest that the role of microglia in ODS is time dependently shifted from detrimental to protective and that astrocytes play a protective role at the late phase. Modulation of excessive proinflammatory responses in microglia during the early phase after rapid correction may represent a therapeutic target for ODS. (C)2010 Wiley-Liss. Inc.

    DOI: 10.1002/glia.21114

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  23. Pathway analysis of single-microglia gene-expression profiles reveals the new molecular targets of minocycline treatment Invited Reviewed

    Suzuki Haruyuki, Sugimura Yoshihisa, Iwama Shintaro, Suzuki Hiromi, Takagi Hiroshi, Kiyota Atsushi, Fukuoka Kazuki, Sawada Makoto, Oiso Yutaka

    NEUROSCIENCE RESEARCH   Vol. 71   page: E223 - E223   2011

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    DOI: 10.1016/j.neures.2011.07.969

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  24. Brain-Targeting DDS with Microglia without Destruction of Blood-Brain Barrier Invited Reviewed

    Sawada Makoto, Suzuki Hiromi, Ono Kenji

    Journal of Pharmaceutical Science and Technology, Japan   Vol. 71 ( 5 ) page: 259 - 267   2011

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    DOI: 10.14843/jpstj.71.259

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  25. Visualization of iNOS gene expression from activated cells in magnetic resonance imaging Invited Reviewed International journal

    Kenji Ono, Kaori Tabata, Hiromi Suzuki, Makoto Sawada

    NEUROSCIENCE RESEARCH   Vol. 71   page: E96 - E96   2011

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    DOI: 10.1016/j.neures.2011.07.413

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  26. Minocycline Prevents Osmotic Demyelination Syndrome by Inhibiting the Activation of Microglia Invited Reviewed

    Suzuki Haruyuki, Sugimura Yoshihisa, Iwama Shintaro, Suzuki Hiromi, Nobuaki Ozaki, Nagasaki Hiroshi, Arima Hiroshi, Sawada Makoto, Oiso Yutaka

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   Vol. 21 ( 12 ) page: 2090 - 2098   2010.12

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    DOI: 10.1681/ASN.2010040438

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  27. Electrosprayed Synthesis of Red-Blood-Cell-Like Particles with Dual Modality for Magnetic Resonance and Fluorescence Imaging Reviewed

    Koichiro Hayashi, Kenji Ono, Hiromi Suzuki, Makoto Sawada, Makoto Moriya, Wataru Sakamoto, Toshinobu Yogo

    SMALL   Vol. 6 ( 21 ) page: 2384 - 2391   2010.11

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    Red blood cells (RBCs) are able to avoid filtration in the spleen to prolong their half-time in the body because of their flexibility and unique shape, or a concave disk with diameter of some 10 mu m. In addition, they can flow through capillary blood vessels, which are smaller than the diameter of RBCs, by morphing into a parachute-like shape. In this study, flexible RBC-like polymer particles are synthesized by electrospraying based on electrospinning. Furthermore, magnetite nanoparticles and fluorescent dye are encapsulated in the particles via in situ hydrolysis of an iron-organic compound in the presence of celluloses. The superparamagnetic behavior of the particles is confirmed by low-temperature magnetic measurements. The particles exhibited not only a dark contrast in magnetic resonance imaging (MRI), but also effective fluorescence. The RBC-like particles with flexibility are demonstrated to have a dual-modality for MRI and fluorescence imaging.

    DOI: 10.1002/smll.201000399

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  28. Correlation between FEPPA uptake and microglia activation in 6-OHDA injured rat brain Invited Reviewed

    Kentaro Hatano, Takashi Yamada, Hiroshi Toyama, Gen Kudo, Masahiko Nomura, Hiromi Suzuki, Masanori Ichise, Alan A. Wilson, Makoto Sawada, Takashi Kato, Kengo Ito

    NEUROIMAGE   Vol. 52   page: S138 - S138   2010.8

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    DOI: 10.1016/j.neuroimage.2010.04.112

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  29. High-frequency, magnetic-field-responsive drug release from magnetic nanoparticle/organic hybrid based on hyperthermic effect.

    HAYASHI K, ONO K, SUZUKI H, SAWADA M, MORIYA M, SAKAMOTO W, YOGO T

    ACS applied materials & interfaces   Vol. 2 ( 7 ) page: 1903-1911   2010.7

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  30. One-Pot Biofunctionalization of Magnetic Nanoparticles via Thiol-Ene Click Reaction for Magnetic Hyperthermia and Magnetic Resonance Imaging Invited Reviewed

    Hayashi Koichiro, Ono Kenji, Suzuki Hiromi, Sawada Makoto, Moriya Makoto, Sakamoto Wataru, Yogo Toshinobu

    CHEMISTRY OF MATERIALS   Vol. 22 ( 12 ) page: 3768 - 3772   2010.6

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    DOI: 10.1021/cm100810g

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  31. Delayed neural damage is induced by iNOS-expressing microglia in a brain injury model Invited Reviewed

    Kenji Ono, Hiromi Suzuki, Makoto Sawada

    NEUROSCIENCE LETTERS   Vol. 473 ( 2 ) page: 146 - 150   2010.4

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    Most CNS diseases begin with inflammation with subsequent neural damage eventually occurring; however, the process leading from the onset of inflammation to neural damage remains obscure. We used an artificial brain injury mouse model and examined how neural damage occurred in the brain parenchyma. The damaged area in each mouse was clearly observed by magnetic resonance imaging (MRI), and the progression of damage was observed to occur in a biphasic manner (acute damage, within 1 week; delayed damage, after 2 weeks). We found that the delayed neural damage was absent in iNOS-deficient mice (iNOS-KO mice). Then, we analyzed brain tissues and determined that delayed neural damage was accompanied by an increase in the levels of NO end products and iNOS expression, with accumulation of iNOS-expressing microglia around the injured area. In addition, the expression of IL-1 beta mRNA was increased in areas affected by acute damage, but not in those affected by delayed damage. These findings suggest that delayed neural damage might arise from NO production by iNOS-expressing activated microglia and that such activated microglia might become a therapeutic target for many CNS diseases. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

    DOI: 10.1016/j.neulet.2010.02.041

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  32. Two activated stages of microglia and PET imaging of peripheral benzodiazepine receptors with [^<11>C]PK11195 in rats Invited Reviewed

    ITO Fumitaka, TOYAMA Hiroshi, KUDO Gen, SUZUKI Hiromi, HATANO Kentaro, ICHISE Masanori, KATADA Kazuhiro, ITO Kengo, SAWADA Makoto

      Vol. 24 ( 3 ) page: 163 - 169   2010.4

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  33. Delayed neural damage is induced by iNOS-expressing microglia in a brain injury model Reviewed

    ONO Kenji, SUZUKI Hiromi, SAWADA Makoto

    Neuroscience Letters   Vol. 473 ( 2 ) page: 146-150   2010.4

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  34. Two activated stage of microglia and PET imaging of peripheral benzodiazepine receptors with [11C]PK11195 in rats Invited Reviewed

    Ito F, Toyama H, Kudo G, Suzuki H, Hatano K, Ichise M, Katada K, Ito K, Sawada M

    Ann Nucl Med   Vol. 24 ( 3 ) page: 163 - 169   2010.4

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    OBJECTIVE: The transition of microglia from the normal resting state to the activated state is associated with an increased expression of peripheral benzodiazepine receptors (PBR). The extent of PBR expression is dependent on the level of microglial activation. A PBR ligand, [(11)C]PK11195, has been used for imaging of the activation of microglia in vivo. We evaluated whether [(11)C]PK11195 PET can indicate differences of microglial activation between no treatment and lipopolysaccharide (LPS) treatment in a rat artificial injury model of brain inflammation. METHODS: On day 1, a small aliquot of absolute ethanol was injected into the rat right striatum (ST) to produce artificial brain injury. On day 3, MRI scans were performed to evaluate and select rats showing a similar degree of brain injury. Then LPS or vehicle was administered intraperitoneally. On day 4, PET scans were performed after a bolus injection of [(11)C]PK11195. Eleven rats (7 LPS administered rats, 4 LPS non-administered rats) were evaluated. We used uptake ratios of the integral of right and left striatum from 0 to 60 min as an estimate of PBR distribution volume (V (60)). The number of activated microglia and mRNA expression of inflammatory cytokines (TNFalpha, IL-1beta) were assessed by isolectin-B4 staining and RT-PCR, respectively. RESULTS: Right/left ST V (60) ratios of LPS group were significantly higher than those of non-LPS group (P < 0.03). Although there were no significant differences in the number of activated microglia between the two groups, LPS group showed higher expression of inflammatory cytokines (TNFalpha, IL-1beta) than the non-treated group indicating that further activation was induced by LPS treatment. CONCLUSION: The results suggest that intensity of PBR signals in [(11)C]PK11195 PET may be related to the level of microglial activation rather than the number in activated microglia at least in an artificial brain injury model.

    DOI: 10.1007/s12149-009-0339-0

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  35. Neuroprotective and Neurotoxic Phenotypes of Activated Microglia in Neonatal Mice with Respective MPTP- and Ethanol-Induced Brain Injury. Reviewed

    Sawada H, Suzuki H, Nagatsu T, Sawada M.

    Neuro-degenerative Diseases   Vol. 7 ( 1-3 ) page: 64-67   2010.2

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  36. Minocycline prevents osmotic demyelination syndrome by inhibiting the activation of microglia. Reviewed

    SUZUKI H, SUGIMURA Y, IWAMA S, SUZUKI H, OZAKI N, NAGASAKI H, ARIMA H, SAWADA M, OISO Y.

    Journal of the American Society of Nephrology   Vol. 21 ( 12 ) page: 2090-2098   2010

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  37. Control of activation in ChR2-expressing astrocytes by blue light exposure Invited Reviewed

    Kenji Ono, Madoka Higa, Kaori Tabata, Hiromi Suzuki, Makoto Sawada

    NEUROSCIENCE RESEARCH   Vol. 68   page: E57 - E57   2010

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    DOI: 10.1016/j.neures.2010.07.020

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  38. Neuroprotective and neurotoxic phenotypes of activated microglia in neonatal mice with respective MPTP- and ethanol-induced brain injury. Invited Reviewed

    Sawada H, Suzuki H, Nagatsu T, Sawada M

    Neuro-degenerative diseases   Vol. 7 ( 1-3 ) page: 64 - 7   2010

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    DOI: 10.1159/000285508

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  39. Gene expression profiling of microglia from the demyelinative lesions in osmotic demyelination syndrome rats Invited Reviewed

    Yoshihisa Sugimura, Haruyuki Suzuki, Shintaro Iwama, Hiromi Suzuki, Atsushi Kiyota, Makoto Sawada, Yutaka Oiso

    NEUROSCIENCE RESEARCH   Vol. 68   page: E199 - E199   2010

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    DOI: 10.1016/j.neures.2010.07.2453

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  40. 小動物における定量的画像解析 Invited Reviewed

    外山 宏, 旗野 健太郎, 鈴木 弘美, 工藤 元, 野村 昌彦, 山田 貴史, 木村 裕一, 市瀬 正則, 澤田 誠

    脳循環代謝   Vol. 21   page: 50 - 57   2010

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  41. Isolation of Microglia Subpopulations Invited Reviewed

    Sawada, M; Suzuki, H

    PROTCOLS FOR NEURAL CELL CULTURE, FOURTH EDITION     page: 231 - 239   2010

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    DOI: 10.1007/978-1-60761-292-6_13

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  42. Comparison of [18F]FEPPA and [11C]PBR28, novel peripheral benzodiazepine receptor ligands for PET, in a rat model of neuroinflammation Invited Reviewed

    Toyama, H; Hatano, K; Suzuki, H; Kudo, G; Ichise, M; Wilson, A; Yamada, T; Katada, K; Sawada, M; Ito, K

    JOURNAL OF NUCLEAR MEDICINE   Vol. 50   2009.5

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  43. Protective roles of brain-migrated immature bone marrow cells against NO-dependent neurotoxicity in a brain injury model Invited Reviewed

    Ono Kenji, Yamamoto Naho, Suzuki Hiromi, Sawada Makoto

    NEUROSCIENCE RESEARCH   Vol. 65   page: S43 - S43   2009

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    DOI: 10.1016/j.neures.2009.09.055

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  44. A PRACTICAL PREPARATION OF [18F]FEPPA USING A PROTIC SOLVENT SYSTEM Invited Reviewed

    Hatano, K; Toyama, H; Yamada, T; Kudo, G; Suzuki, H; Ichise, M; Wilson, AA; Sawada, M; Ito, K

    JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS   Vol. 52   page: S273 - S273   2009

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  45. Increase in hemokinin-1 mRNA in the spinal cord during the early phase of a neuropathic pain state

    MATSUMURA T, SAKAI A, NAGANO M, SAWADA M, SUZUKI H, UMINO M, SUZUKI H

    British Journal of Pharmacology   Vol. 155 ( 5 ) page: 767-774   2008.11

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  46. Blockade of microglial glutamate release protects against ischemic brain injury Invited Reviewed

    Hideyuki Takeuchi, Shijie Jin, Hiromi Suzuki, Yukiko Doi, Jianfeng Liang, Jun Kawanokuchi, Tetsuya Mizuno, Makoto Sawada, Akio Suzumura

    EXPERIMENTAL NEUROLOGY   Vol. 214 ( 1 ) page: 144 - 146   2008.11

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    Glutamate released by activated microglia induces excito-neurotoxicity and may contribute to neurodegeneration in numerous neurological diseases including ischemia, inflammation, epilepsy, and neurodegenerative diseases. We observed that the gap junction blocker carbenoxolone (CBX) or the glutaminase inhibitor 6-diazo-5-oxo-i-norleucine (DON) decreased glutamate release from activated microglia and rescued neuronal death in a dose-dependent manner in vitro. In gerbils, treatment with CBX or DON also prevented the delayed death of hippocampal neurons following transient global ischemia. Thus, blockade of microglial glutamate release may be an effective therapeutic strategy against neurodegeneration after ischemic injury. (C) 2008 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.expneurol.2008.08.001

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  47. Increase in hemokinin-1 mRNA in the spinal cord during the early phase of a neuropathic pain state Invited Reviewed

    Matsumura, T; Sakai, A; Nagano, M; Sawada, M; Suzuki, H; Umino, M; Suzuki, H

    BRITISH JOURNAL OF PHARMACOLOGY   Vol. 155 ( 5 ) page: 767 - 774   2008.11

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    DOI: 10.1038/bjp.2008.301

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  48. In vivo imaging of microglial activation using a peripheral benzodiazepine receptor ligand: [11C]PK-11195 and animal PET following ethanol injury in rat striatum. Reviewed

    Toyama H, Hatano K, Suzuki H, Ichise M, Momosaki S, Kudo G, Ito F, Kato T, Yamaguchi H, Katada K, Sawada M, Ito K

    Annals of nuclear medicine   Vol. 22 ( 5 ) page: 417 - 424   2008.6

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    DOI: 10.1007/s12149-008-0136-1

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    CiNii Books

    CiNii Research

  49. Expression of cytokines and neurotrophins after acute subarachnoid hemorrhage Invited Reviewed

    Sehba, FA; Flores, R; Ono, K; Suzuki, H; Sawada, SM; Kanzawa, T

    STROKE   Vol. 39 ( 2 ) page: 650 - 650   2008.2

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  50. Enhancement of glioma formation and growth by brain-migrated immature bone marrow cells Invited Reviewed

    Kenji Ono, Taiki Furukawa, Hiromi Suzuki, Emi Sato, Makoto Sawada

    NEUROSCIENCE RESEARCH   Vol. 61   page: S276 - S276   2008

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  51. 脳の標的化画像診断-PETによる活性化ミクログリアの分子イメージング- Invited Reviewed

    外山 宏, 工藤 元, 伊藤 文隆, 片田 和広, 大橋 正男, 中根 正人, 籏野 健太郎, 加藤 隆司, 伊藤 健吾, 鈴木 弘美, 澤田 誠, 市瀬 正則

    21世紀COE プログラム、超低侵襲標的化診断治療開発センター研究成果報告書     page: 87 - 88   2008

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  52. In-vivo imaging of microglial activation using a novel peripheral benzodiazepine receptor ligand, F-18-FEPPA and animal PET following 6-OHDA injury of the rat striatum; A comparison with C-11-PK11195 Invited Reviewed

    Kudo Gen, Toyama H., Hatano K., Suzuki H., Wilson A. A., Ichise M., Ito F., Kato T., Katada K., Sawada M., Ito K.

    NEUROIMAGE   Vol. 41   page: T94 - T94   2008

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    DOI: 10.1016/j.neuroimage.2008.04.063

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  53. 動物PETによるラット線状体障害モデルにおけるミクログリア毒性転換の検討 Invited Reviewed

    鈴木 弘美, 外山 宏, 籏野 健太郎, 工藤 元, 伊藤 文隆, 小野 健治, 加藤 隆司, 伊藤 健吾, 澤田 誠

    バイオイメージング   Vol. 16 ( 2 ) page: 93 - 94   2007.10

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  54. N-benzyl-2-(6,8-dichloro-2-(4-chlorophenyl)imidazo[1,2-a]pyridin-3-yl)-N-(6-(7-nitrobenzo[c][1,2,5]oxadiazol-4-ylamino)hexyl)acetamide as a new fluorescent probe for peripheral benzodiazepine receptor and microglial cell visualization. Invited Reviewed

    Laquintana V, Denora N, Lopedota A, Suzuki H, Sawada M, Serra M, Biggio G, Latrofa A, Trapani G, Liso G

    Bioconjugate chemistry   Vol. 18 ( 5 ) page: 1397 - 407   2007.9

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    DOI: 10.1021/bc060393c

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  55. Activated microglia affect the nigro-striatal dopamine neurons differently in neonatal and aged mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine Reviewed

    Hirohide Sawada, Ryohei Hishida, Yoko Hirata, Kenji Ono, Hirorni Suzuki, Shin-ichi Muramatsu, Imaharu Nakano, Toshiharu Nagatsu, Makoto Sawada

    JOURNAL OF NEUROSCIENCE RESEARCH   Vol. 85 ( 8 ) page: 1752 - 1761   2007.6

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    Microglia play an important role in the inflammatory process that occurs in Parkinson's disease (PD). Activated microglia produce cytokines and neurotrophins and may have neurotoxic or neurotrophic effects. Because microglia are most proliferative and easily activated during the neonatal period, we examined the effects of neonatal microglia activated with lipopolysaccharide (LPS) on the nigro-striatal dopamine neurons in mice treated with 1-methyl-4-phenyl-1 2,3,6-tetrahyd ropyridine (MPTP), in comparison with activated microglia from the aged mice. By MPTP administration to neonatal mice, the number of dopamine neurons in the substantia nigra (SN) was decreased significantly, whereas that in the mice treated with LPS and MPTP was recovered to normal, along with significant microglial activation. Tyrosine hydroxylase (TH) activity, the levels of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC), and the levels of pro-inflammatory cytokines IL-1 beta and IL-6 in the midbrain were elevated in the neonates treated with LPS and MPTR On the contrary, although the number of dopamine neurons in the 60-week-old mice treated with MPTP was also decreased significantly, the microglial activation by LPS treatment caused a further decrease in their number. These results suggest that the activated microglia in neonatal mice are different from those in aged mice, with the former having neurotrophic potential toward the dopamine neurons in the SN, in contrast to the neurotoxic effect of the latter. (c) 2007 Wiley-Liss, Inc.

    DOI: 10.1002/jnr.21241

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    J-GLOBAL

  56. Neuroprotective effect of exogenous microglia in global brain ischemia. Invited Reviewed

    Imai F, Suzuki H, Oda J, Ninomiya T, Ono K, Sano H, Sawada M

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism   Vol. 27 ( 3 ) page: 488 - 500   2007.3

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    DOI: 10.1038/sj.jcbfm.9600362

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  57. [Targeting and imaging of brain-specific cell migration]. Invited Reviewed

    Sawada M, Ono K, Suzuki H

    Nihon rinsho. Japanese journal of clinical medicine   Vol. 65 ( 2 ) page: 213 - 8   2007.2

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  58. P2-16 新生時由来ミクログリアの活性化がパーキンソン病モデルマウスの黒質ドーパミンニューロンに対して神経保護的にはたらく可能性(脳神経,一般演題,第48回日本組織細胞化学会総会(第8回日中合同組織細胞化学セミナー) 第39回日本臨床分子形態学会総会 合同学術集会) Invited Reviewed

    澤田 浩秀, 菱田 良平, 平田 洋子, 小野 健治, 鈴木 弘美, 村松 慎一, 中野 今治, 永津 俊治, 澤田 誠

    日本組織細胞化学会総会プログラムおよび抄録集   ( 48 )   2007

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  59. アルツハイマー病早期診断マーカーのための活性化ミクログリアの画像化-PETによる末梢性ベンゾジアゼピン受容体イメージング- Invited Reviewed

    外山 宏, 工藤 元, 伊藤 文隆, 片田 和広, 大橋 正男, 中根 正人, 籏野 健太郎, 加藤 隆司, 伊藤 健吾, 鈴木 弘美, 澤田 誠, 市瀬 正則

    医科学応用研究財団研究報告 26     page: 415 - 420   2007

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    CiNii Research

  60. The intra-arterial injection of microglia protects hippocampal CA1 neurons against global ischemia-induced functional deficits in rats Invited Reviewed

    Y. Hayashi, Y. Tomimatsu, H. Suzuki, J. Yamada, Z. Wu, H. Yao, Y. Kagamiishi, N. Tateishi, M. Sawada, H. Nakanishi

    NEUROSCIENCE   Vol. 142 ( 1 ) page: 87 - 96   2006.9

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    In the present study, we have attempted to elucidate the effects of the intra-arterial injection of microglia on the global ischemia-induced functional and morphological deficits of hippocampal CA1 neurons. When PKH26-labeled immortalized microglial cells, GMIR1, were injected into the subclavian artery, these exogenous microglia were found to accumulate in the hippocampus at 24 h after ischemia. In hippocampal slices prepared from medium-injected rats subjected to ischemia 48 h earlier, synaptic dysfunctions including a significant reduction of synaptic responses and a marked reduction of long-term potentiation (LTP) of the CA3-CA1 Schaffer collateral synapses were observed. At this stage, however, neither significant neuronal degeneration nor gliosis was observed in the hippocampus. At 96 h after ischemia, there was a total loss of the synaptic activity and a marked neuronal death in the CA1 subfield. In contrast, the basal synaptic transmission and LTP of the CA3-CA1 synapses were well preserved after ischemia in the slices prepared from the microglia-injected animals. We also found the microglial-conditioned medium (MCM) to significantly increase the frequency of the spontaneous postsynaptic currents of CA1 neurons without affecting the amplitude, thus indicating that MCM increased the provability of the neurotransmitter release. The protective effect of the intra-arterial injected microglia against the ischemia-induced neuronal degeneration in the hippocampus was substantiated by immunohistochemical and immunoblot analyses. Furthermore, the arterial-injected microglia prevented the ischemia-induced decline of the brain-derived neurotrophic factor (BDNF) levels in CA1 neurons. These observations strongly suggest that the arterial-injection of microglia protected CA1 neurons against the ischemia-induced neuronal degeneration. The restoration of the ischemia-induced synaptic deficits and the resultant reduction of the BDNF levels in CA1 neurons, possibly by the release of diffusible factor(s), might thus contribute to the protective effect of the arterial-injection of microglia against ischemia-induced neuronal degeneration. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.neuroscience.2006.06.003

    Web of Science

    PubMed

  61. The intra-arterial injection of microglia protects hippocampal CA1 neurons against global ischemia-induced functional deficits in rats

    HAYASHI Y, TOMIMATSU Y, SUZUKI H, YAMADA J, WU Z, YAO H, KAGAMIISI Y, TAKEISHI N, SAWADA M, NAKANISHI H

    Neuroscience   Vol. 142 ( 1 ) page: 87-96   2006.9

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  62. Modulations of muscle protein metabolism by branched-chain amino acids in normal and muscle-atrophying rats. Invited Reviewed

    Kobayashi H, Kato H, Hirabayashi Y, Murakami H, Suzuki H

    The Journal of nutrition   Vol. 136 ( 1 Suppl ) page: 234S - 6S   2006.1

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    DOI: 10.1093/jn/136.1.234S

    PubMed

  63. Activated microglia affect the nigro-striatal dopamine neurons differently in neonatal and aged mice treated with MPTP Invited Reviewed

    Hirohide Sawada, Ryohei Hishida, Yoko Hirata, Kenji Ono, Hiromi Suzuki, Shin-ichi Muramatsu, Imaharu Nakano, Kunihiro Tsuchida, Toshiharu Nagatsu, Makoto Sawada

    NEUROSCIENCE RESEARCH   Vol. 55   page: S201 - S201   2006

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  64. In vivo imaging of microglial activation using a peripheral benzodiazepine receptor ligand, [11C]PK11195 and animal PET following implantation of cultured activated microglia into rat striatum Invited Reviewed

    Kudo, G; Toyama, H; Hatano, K; Suzuki, H; Ichise, M; Ito, F; Kato, T; Sawada, M; Katada, K; Ito, K

    NEUROIMAGE   Vol. 31   page: T148 - T148   2006

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    DOI: 10.1016/j.neuroimage.2006.04.131

    Web of Science

  65. 活性型ミクログリアの In Vivo イメージング Invited Reviewed

    鈴木 弘美, 外山 宏, 工藤 元, 籏野 健太郎, 関亦 克彦, 小野 健治, 中根 正人, 加藤 隆司, 伊藤 健吾, 澤田 誠

    バイオイメージング   Vol. 14 ( 3 ) page: 129 - 130   2005.9

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    Authorship:Lead author, Corresponding author   Language:Japanese   Publishing type:Research paper (scientific journal)  

    CiNii Research

  66. A lentiviral expression system demonstrates that L*protein of Theiler's murine encephalomyelitis virus(TMEV) is essential for virus growth in a murine macrophage-like cell line.

    HIMEDA T, OHARA Y, ASAKURA K, KONTANI Y, MURAKAMI M, SUZUKI H, SAWADA M

    Virus Research   Vol. 108 ( 1-2 ) page: 23-28   2005.3

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  67. Cytokine production of activated microglia and decrease in neurotrophic factors of neurons in the hippocampus of Lewy body disease brains.

    IMAMURA K, HISHIKAWA N, ONO K,SUZUKI H, SAWADA M, NAGATSU T, YOSHIDA M, HASHIZUME Y

    Acta Neuropathologica   Vol. 109 ( 2 ) page: 141-150   2005.2

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  68. Cytokine production of activated microglia and decrease in neurotrophic factors of neurons in the hippocampus of Lewy body disease brains Invited Reviewed

    K Imamura, N Hishikawa, K Ono, H Suzuki, M Sawada, T Nagatsu, M Yoshida, Y Hashizume

    ACTA NEUROPATHOLOGICA   Vol. 109 ( 2 ) page: 141 - 150   2005.2

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    Dementia is a frequent complication of Parkinson's disease (PD) and usually occurs late in the protracted course of the illness. We have already reported numerous MHC class II-positive microglia in the hippocampus in PD patients, and that this phenomenon may be responsible for functional changes in the neurons and the cognitive decline in PD patients. In this study, we have investigated the distribution of activated microglia and the immunohistochemical and the mRNA expression of several cytokines and neurotrophic factors of the hippocampus in PD and dementia with Lewy bodies (DLB). The brains from five cases of PD and five cases of DLB that were clinically and neuropathologically diagnosed, and those from four normal controls (NC) were evaluated by immunohistochemistry using anti-HLA-DP, -DQ, -DR (CR3/43), anti-alpha-synuclein, anti-brain-derived neurotrophic factor (BDNF), and anti-glial fibrillary acidic protein antibodies. In addition, the mRNA expressions of cytokines (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, TGF-beta) and neurotrophic factors (BDNF, GDNF, NGF, NT-3) of these brains were evaluated by the reverse transcription-PCR method. MHC class II-positive microglia were distributed diffusely in the hippocampus of PD and DLB brains. Although the cytoplasm of pyramidal and granular cells of the hippocampus in NC brains was strongly stained by anti-BDNF antibodies, it was only weakly stained in PD and DLB brains. The mRNA expression of IL-6 was significantly increased in the hippocampus of PD and DLB brains, and that of BDNF was significantly decreased in the hippocampus of DLB brains. The increased number of activated microglia and the production of neurotrophic cytokines such as IL-6, together with the decreased expression of the neurotrophic factors of neurons in the hippocampus of PD and DLB brains, may be related to functional cellular changes associated with dementia.

    DOI: 10.1007/s00401-004-0919-y

    Web of Science

  69. Murine lymph node-derived stromal cells effectively support survival but induce no activation/proliferation of peripheral resting T cells in vitro Invited Reviewed

    Zhou YW, Aritake S, Endharti AT, Wu JH, Hayakawa A, Nakashima I, Suzuki H

    IMMUNOLOGY   Vol. 109 ( 4 ) page: 496 - 503   2003.8

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  70. Preservation of hematopoietic properties in transplanted bone marrow cells in the brain. Invited Reviewed

    Ono K, Yoshihara K, Suzuki H, Tanaka KF, Takii T, Onozaki K, Sawada M

    Journal of neuroscience research   Vol. 72 ( 4 ) page: 503 - 7   2003.5

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    DOI: 10.1002/jnr.10588

    PubMed

  71. Existence of functional beta(1)- and beta(2)-adrenergic receptors on microglia

    KF Tanaka, H Kashima, H Suzuki, K Ono, M Sawada

    JOURNAL OF NEUROSCIENCE RESEARCH   Vol. 70 ( 2 ) page: 232 - 237   2002.10

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    We examined the expression and function of beta-adrenergic receptor (beta-AR) subtypes in both isolated primary rat microglia and a rat microglial cell line. RTPCR analyses revealed that microglia expressed beta(1)- and beta(2)-ARs but not beta(3)-ARs, whereas rat primary peritoneal macrophages expressed only beta(2)-ARs. Stimulation of beta-ARs on microglia by norepinephrine (NE) resulted in an increase in the level of intracellular cAMP and the subsequent expression of interleukin-1beta mRNA. These effects were prevented by propranolol. Similar results were obtained with other selective beta(1)-AR agonists and antagonists. beta(2)-ARs on microglia were also functional. It is possible that noradrenergic innervations participate in the control of microglial functions via beta(1)-ARs on microglia in the brain, because NE has high affinity for beta(1)- and beta(3)-ARs but little or no affinity for beta(2)-ARs. It seems physiologically significant that microglia can be controlled by NE, which predominates over epinephrine in the brain, whereas macrophages in peripheral tissues can be controlled by epinephrine, which is at higher levels in peripheral tissues. (C) 2002 Wiley-Liss, inc.

    DOI: 10.1002/jnr.10399

    Web of Science

  72. Modes of activation of mitogen-activated protein kinases and their roles in cepharanthine-induced apoptosis in human leukemia cells Invited Reviewed

    Wu JH, Suzuki H, Akhand AA, Zhou YW, Hossain K, Nakashima I

    CELLULAR SIGNALLING   Vol. 14 ( 6 ) page: 509 - 515   2002.6

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  73. Brain-specific migration and protective roles in brain damage of microglia - A new therapeutic approach for catecholamine neuronal disfunctions Reviewed

    M Sawada, F Imai, H Suzuki

    CATECHOLAMINE RESEARCH: FROM MOLECULAR INSIGHTS TO CLINICAL MEDICINE   Vol. 53   page: 217 - 220   2002

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    Language:English   Publishing type:Research paper (international conference proceedings)   Publisher:KLUWER ACADEMIC/PLENUM PUBL  

    Web of Science

  74. Preservation of neurotophin expression in microglia that migrate into the gerbil's brain across the blood-brain barrier.

    SUZUKI H, IMAI F, KANNO T, SAWADA M

    Neuroscience Letters   Vol. 312 ( 2 ) page: 95-98   2001.10

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  75. Osmotic stress-mediated activation of RET kinases involves intracellular disulfide-bonded dimer formation Invited Reviewed

    Takeda K, Kato M, Wu JH, Iwashita T, Suzuki H, Takahashi M, Nakashima I

    ANTIOXIDANTS & REDOX SIGNALING   Vol. 3 ( 3 ) page: 473 - 482   2001.6

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  76. 4-hydroxynonenal induces a cellular redox status-related activation of the caspase cascade for apoptotic cell death. Invited Reviewed

    Liu W, Kato M, Akhand AA, Hayakawa A, Suzuki H, Miyata T, Kurokawa K, Hotta Y, Ishikawa N, Nakashima I

    Journal of cell science   Vol. 113 ( Pt 4)   page: 635 - 41   2000.2

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    DOI: 10.1242/jcs.113.4.635

    PubMed

  77. Molecular Mechanism of Activation and Superactivation of Ret Tyrosine Kinases by Ultraviolet Light Irradiation Invited Reviewed

    Kato Masashi, Iwashita Toshihide, Akhand Anwarul A., Liu Wei, Takeda Kozue, Takeuchi Kei, Yoshihara Motoi, Hossain Khaled, Wu Jianghong, Du Jun, Oh Chanho, Kawamoto Yoshiyuki, Suzuki Haruhiko, Takahashi Masahide, Nakashima Izumi

    ANTIOXIDANTS & REDOX SIGNALING   Vol. 2 ( 4 ) page: 841 - 850   2000

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  78. Normal regulatory alpha/beta T cells effectively eliminate abnormally activated T cells lacking the interleukin 2 receptor beta in vivo Invited Reviewed

    Suzuki H, Zhou YW, Kato M, Mak TW, Nakashima I

    JOURNAL OF EXPERIMENTAL MEDICINE   Vol. 190 ( 11 ) page: 1561 - 1571   1999.12

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  79. Exogenous microglia enter the brain and migrate into ischaemic hippocampal lesions.

    IMAI F, SAWADA M, SUZUKI H, ZLOKOVIC BV, KOJIMA J, KUNO S, NAGATSU T, NITATORI T, UCHIYAMA Y, KANNNO T

    Neuroscience Letters   Vol. 272 ( 2 ) page: 127-130   1999.9

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  80. Exogenous microglia enter the brain and migrate into ischaemic hippocampal lesions

    F Imai, M Sawada, H Suzuki, BV Zlokovic, J Kojima, S Kuno, T Nagatsu, T Nitatori, Y Uchiyama, T Kanno

    NEUROSCIENCE LETTERS   Vol. 272 ( 2 ) page: 127 - 130   1999.9

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    We compared migration of systemically injected microglia into normal brain vs. ischaemic brain using a model of ischaemic hippocampal lesion. Microglia were labeled by a fluorescent dye using our standard phagocytosis procedure of microscopic particles and then injected intra-arterially into Mongolian gerbils subjected to ischaemia reperfusion neuronal injury. Delayed death of pyramidal neurons was confirmed by conventional histological analysis and dUTP nick end labeling (TUNEL) method. Clusters of dye-tagged cells migrating into the hippocampal ischaemic lesions were confirmed histochemically to be microglia. Since peripherally injected microglia exhibit specific affinity for ischaemic brain lesions and does not exacerbate ischaemic neuronal injury in the present model, we suggest that microglia may have a potential to be used as a piggy-back ride to deliver therapeutic genes and/or drugs for CNS repair following transitory global ischaemic insult. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

    DOI: 10.1016/S0304-3940(99)00592-3

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    PubMed

  81. Brain-specific gene expression by immortalized microglia cell-mediated gene transfer in the mammalian brain

    SAWADA M, IMAI F, SUZUKI H. HAYAKAWA M, KANNO T, NAGATSU T

    FEBS Letters   Vol. 433 ( 1-2 ) page: 37-40   1998.8

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  82. Migration activity of microglia and macrophages into rat brain.

    IMAI F, SAWADA M, SUZUKI H, KIYA N, HAYAKAWA M,NAGATSU T, MARUNOUCHI T, KANNO T

    Neuroscience Letters   Vol. 237 ( 1 ) page: 49-52   1997.11

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Books 7

  1. PET/CT for Inflammatory Diseases: Basic Sciences, Typical Cases, and Review Reviewed

    Hiromi Suzuki, Makoto Sawada( Role: Contributor ,  Role of Microglia in Neuroinflammation)

    Springer  2020.2  ( ISBN:978-981-15-0810-3

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    Total pages:234   Language:English Book type:Textbook, survey, introduction

    At present, common diseases of CNS were often chronic and progressive which could affect the patient's quality of life seriously. But the pathogenesis for most of them had not been fully understood and was no effective pre- vention or treatment. Certain pathological injury could cause cellular inflammatory response. Microglia, the first activated effector cells, played an important role in the immune defense process. Microglia had a two-way effect. On the one hand, activated microglia phagocytosed damaged cell debris and removed antigenic substances, and could release cyto- toxic factors which would aggravate the injury of neuron. On the other hand, activated microglia may accumulate around damaged neurons and might induce neurotrophin-dependent protective activity. Therefore, to study the mechanism of microglia in the diseases of CNS and limit their effects on neuronal injury may help to retard the procession of some chronic disease and enhance the therapeutic effect of acute CNS diseases. Microglia are expected to become a new tar- get for the treatment of neurodegenerative diseases and cen- tral nervous system diseases.

  2. アルツハイマー病 発症メカニズムと新規診断法・創薬・治療開発

    澤田 誠, 鈴木弘美( Role: Joint author)

    株式会社エヌ・ティ・エス  2018.8  ( ISBN:978-4-86043-578-3

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    Total pages:460   Language:Japanese Book type:Textbook, survey, introduction

  3. 脳卒中病態学のススメ・脳内マクロファージとミクログリア

    澤田 誠, 鈴木弘美( Role: Joint author)

    南山堂  2018.2  ( ISBN:978--4-525-24851-2

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  4. Etiology and Pathophysiology of Parkinson's Disease: Role of microglia in inflammatory process, in Parkinson's disease

    Sawada H, Suzuki H, Ono K, Imamaura K, Nagatsu T, Sawada M( Role: Joint author)

    InTech  2011.10  ( ISBN:978-953-307-462-7

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  5. 遺伝子医学MOOK: 小動物PETによるラットパーキンソン病モデルの神経傷害性と治療効果判定

    外山 宏、籏野健太郎、鈴木弘美( Role: Joint author)

    メディカルドゥ  2010.10 

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  6. 脳循環代謝: 小動物における定量的画像解析

    外山宏、籏野健太郎、鈴木弘美、工藤元、野村昌彦、山田貴史、木村裕一、市瀬正則、澤田誠( Role: Joint author)

    日本脳循環代謝学会  2010.7 

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  7. Protocols for Neural Cell Culture・Isolation of microglia subpopulations

    SAWADA Makoto, SUZUKI Hiromi( Role: Joint author)

    Humana Press  2009 

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MISC 18

  1. LC-MS/MS imaging with thermal film-based laser microdissection Reviewed

    Michiko Oya, Hiromi Suzuki, Andrea Roxanne, J. Anas, Koichi Oishi, Kenji Ono, Shun Yamaguchi, Megumi Eguchi, Makoto Sawada

    Anal Bioanal Chem   Vol. 410 ( 2 ) page: 491 - 499   2018.1

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    DOI: 10.1007/s00216-017-0739-2.

  2. Visualization of iNOS gene expression from activated cells in magnetic resonance imaging

    Kenji Ono, Kaori Tabata, Hiromi Suzuki, Makoto Sawada

    NEUROSCIENCE RESEARCH   Vol. 71   page: E96 - E96   2011

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    DOI: doi.org/10.1016/j.neures.2011.07.413

  3. Inducible nitric oxide synthase during the late phase of sepsis is associated with hypothermia and immune cell migration Reviewed

    Laboratory Investigation   Vol. 98 ( 5 ) page: 629 - 639   2018.5

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    DOI: 10.1038/s41374-018-0021-z

  4. Optogenetic control of cell differentiation in channelrhodopsin-2-expressing OS3, a bipotential glial progenitor cell line Reviewed International journal

    Kenji Ono, Hiromi Suzuki, Ryusei Yamamoto, Hideki Sahashi, Yuhei Takido, Makoto Sawada

    NEUROCHEMISTRY INTERNATIONAL   Vol. 104   page: 49 - 63   2017.3

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    Alterations in the intracellular ion environment have been identified as one of the signals playing a critical role in the control of cellular proliferation and differentiation; however, the mechanisms responsible for signal transduction remain unclear. Recent studies have reported that channelrhodopsin-2 (ChR2) is a rapidly gated blue light (BL)-sensitive cation channel suitable for the non-invasive control of ion influx. We herein examined the expression of differentiation-associated markers by photo-activation and its signal transduction in ChR2-expressing OS3 (OS3ChR2) cells, which are clonal bipotential glial progenitor cells. Increases were observed in intracellular Na+ and Ca2+ concentrations in OS3ChR2 cells with BL exposure. Alterations in the intracellular ion environment, particularly in Ca2+, led to increases in the expression of oligodendrocyte markers including galactocerebrosides (GalC) and decreases in that of astrocyte markers such as glial fibrillary acidic protein (GFAP). These alterations also triggered activation of the ERK1/2 signaling pathway, which is involved in cell survival, and PI3K/Akt/mTOR signaling pathway, which is involved in oligodendrocyte differentiation, characterized by GalC expression. Moreover, when photo-activated OS3ChR2 cells were injected into mice with lysophosphatidyl choline (LPC)-induced demyelination, deficits in motor function were reduced. Our results demonstrated that signal transduction by ChR2-expressing glial progenitor cells may be controlled through alterations induced in the intracellular ion environment by photo-activation and results in oligodendrOcyte differentiation from glial progenitor cells. Our results also suggest that ChR2-expressing glial progenitor cells have potential as a useful tool for therapeutic approaches to brain and spinal cord disorders associated with oligodendrocyte dysfunctions. (C) 2017 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.neuint.2016.12.022

  5. ミクログリアによるBBB非崩壊型の脳へのターゲティングDDS Invited

    澤田 誠, 鈴木弘美, 小野健治

    薬剤学   Vol. 71 ( 5 ) page: 259-267   2011

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  6. Control of activation in ChR2-expressing astrocytes by blue light exposure

    Kenji Ono, Madoka Higa, Kaori Tabata, Hiromi Suzuki, Makoto Sawada

      Vol. 68   page: E57 - E57   2010.7

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    DOI: doi.org/10.1016/j.neures.2010.07.020

  7. Gene expression profiling of microglia from the demyelinative lesions in osmotic demyelination syndrome rats

    Yoshihisa Sugimura, Haruyuki Suzuki, Shintaro Iwama, Hiromi Suzuki, Atsushi Kiyota, Makoto Sawada, Yutaka Oiso

    NEUROSCIENCE RESEARCH   Vol. 68   page: E199 - E199   2010.7

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    DOI: doi.org/10.1016/j.neures.2010.07.2453

  8. Delayed neural damage is induced by iNOS-expressing microglia in a brain injury model Reviewed

    Kenji Ono, Hiromi Suzuki, Makoto Sawada

    NEUROSCIENCE LETTERS   Vol. 473 ( 2 ) page: 146 - 150   2010.1

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    DOI: 10.1016/j.neulet.2010.02.04

  9. 動物PETによるラット線状体障害モデルにおけるミクログリア毒性転換の検討

    鈴木 弘美, 外山 宏, 籏野 健太郎, 工藤 元, 伊藤 文隆, 小野 健治, 加藤 隆司, 伊藤 健吾, 澤田 誠

    バイオイメージング   Vol. 16 ( 2 ) page: 93 - 94   2007.10

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    CiNii Books

  10. 細胞を用いた脳の標的化とその画像化

    澤田 誠, 小野健治, 鈴木弘美

    日本臨床   Vol. 65 ( 2 ) page: 213-218   2007.2

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    本論文では、脳選択的移行能を有するミクログリアや一部の骨髄細胞を用いた脳の標的化技術と近赤外波長域蛍光色素を組み合わせたin vivo imagingについて述べている。

  11. 活性型ミクログリアの In Vivo イメージング

    鈴木 弘美, 外山 宏, 工藤 元, 籏野 健太郎, 関亦 克彦, 小野 健治, 中根 正人, 加藤 隆司, 伊藤 健吾, 澤田 誠

    バイオイメージング   Vol. 14 ( 3 ) page: 129 - 130   2005.9

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    CiNii Books

  12. A lentiviral expression system demonstrates that L* protein of Theiler's murine encephalomyelitis virus (TMEV) is essential for virus growth in a murine macrophage-like cell line Reviewed

    HIMEDA Toshiki, OHARA Yoshiro, ASAKURA Kunihiko, KONTANI Yasuhide, MURAKAMI Manabu, SUZUKI Hiromi, SAWADA Makoto

    Virus Research   Vol. 108   page: 23-28 - 28   2005

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    The DA subgroup strains of Theiler&#039;s murine encephalomyelitis virus (TMEV) synthesize L* protein, which is translated out of frame with the polyprotein from an alternative AUG, 13 nucleotides downstream from the authentic polyprotein AUG. By a &#039;loss of function&#039; experiment using a mutant virus, DAL*-1, in which the L* AUG is mutated to an ACG, L* protein is shown to play an important role in virus persistence, TMEV-induced demyelination, and virus growth in macrophages. In the present study, we established an L* protein-expressed macrophage-like cell line and confirmed the importance of L* protein in virus growth in this cell line.

  13. 活性型ミクログリアの In Vivo イメージング

    鈴木 弘美, 外山 宏, 工藤 元, 籏野 健太郎, 小野 健治, 中根 正人, 桃崎 壮太郎, 加藤 隆司, 伊藤 健吾, 澤田 誠

    バイオイメージング   Vol. 13 ( 3 ) page: 184 - 185   2004.10

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    Language:Japanese  

    CiNii Books

  14. 脳機能障害とミクログリアのかかわりおよび細胞を用いた標的化治療・診断 (バイオイメージングが切り開くあらたな診断・治療評価技術)

    鈴木 弘美, 澤田 誠

    医学のあゆみ   Vol. 210 ( 3 ) page: 187 - 190   2004.7

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    Language:Japanese   Publisher:医歯薬出版  

    CiNii Books

    Other Link: http://search.jamas.or.jp/link/ui/2005023766

  15. 脳・神経系に特異的な細胞浸潤のイメージング

    鈴木 弘美, 澤田 誠

    バイオイメージング   Vol. 12 ( 3 ) page: 259 - 260   2003.12

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    Language:Japanese  

    CiNii Books

  16. ミクログリアにはbeta2アドレナリン受容体に加えbeta1アドレナリン受容体も発現している

    田中 謙二, 浅井 昌弘, 鈴木 弘美, 小野 健治, 澤田 誠

    神経化学   Vol. 39 ( 3 ) page: 329 - 329   2000.10

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    Language:Japanese   Publisher:日本神経化学会  

  17. Development of a brain-targetted cell therapy using microglia as a vehicle: Application to ischaemia

    F Imai, M Sawada, H Suzuki, T Kanno

    BRAIN PATHOLOGY   Vol. 10 ( 4 ) page: 564 - 564   2000.9

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    Language:English   Publishing type:Research paper, summary (international conference)   Publisher:INT SOC NEUROPATHOLOGY  

    Web of Science

  18. Brain-specific gene expression by immortalized microglial cell-mediated gene transfer in the mammalian brain

    M Sawada, F Imai, H Suzuki, M Hayakawa, T Kanno, T Nagatsu

    FEBS LETTERS   Vol. 433 ( 1-2 ) page: 37 - 40   1998.8

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    Language:English   Publisher:ELSEVIER SCIENCE BV  

    The intra-arterial injection of immortalized microglia transfected with the lacZ gene, resulted in the expression of beta-galactosidase in the rat brain at 48 h and the activity of beta-galactosidase was detected for up to 3 weeks post-injection. More than 30-fold higher activity of beta-galactosidase was detected in the brain than in the liver, lung or spleen at 48 h post-injection. This method allows us to easily deliver the gene of interest to the brain without influencing other organs. Our brain-targeting gene delivery system can facilitate gene therapy of several brain disorders, including brain tumor, metabolic disorders, and degenerative disorders, as well as investigation into the roles of particular genes in brain function and development. (C) 1998 Federation of European Biochemical Societies.

    DOI: 10.1016/S0014-5793(98)00879-5

    Web of Science

    PubMed

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Presentations 84

  1. Detection of activated microglia by mass spectrometry imaging

    Hiromi Suzuki, Kenji Ono, Makoto Sawada

    2022.11.30 

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    Event date: 2022.11 - 2022.12

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  2. エクソソームを介したシグナルペプチドの細胞外放出

    小野健治、丹羽幹夫、鈴木弘美、小林ベイリー菜穂子、吉田徹彦、澤田 誠

    第95回日本生化学会大会   2022.11.9  名古屋大学 門松健治

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    Event date: 2022.11

    Language:Japanese  

    Venue:名古屋   Country:Japan  

  3. LC-MS/MS-SRMを用いた、マウス脳組織中のTSPOリガンドPK11195とFEPPAの同時定量

    4. ANAS Jocsing, 鈴木弘美, 小野健治, 外山 宏, 野村昌彦, 籏野健太郎,原田健一, 澤田 誠

    日本薬学会142年会  2022.3.26  名城大学 森 裕二

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    Event date: 2022.3

    Language:English   Presentation type:Poster presentation  

    Venue:Web開催   Country:Japan  

  4. 質量分析イメージングによる脳内神経炎症の検出の試み

    鈴木弘美, 藤田爽加, 小野健治, 澤田 誠

    第44回分子生物学会年会  2021.12.2 

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    Event date: 2021.12

    Language:Japanese   Presentation type:Poster presentation  

    Venue:横浜 みなとみらい   Country:Japan  

  5. オリゴデンドロサイトへ分化誘導したグリア前駆細胞から放出されるエクソソームの解析

    小野健治, 伊藤友香, 大橋和哉, 鈴木弘美, 澤田 誠

    第94回日本生化学会大会  2021.11  筑波大学 深水昭吉

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    Event date: 2021.11

    Language:English   Presentation type:Poster presentation  

    Venue:Web開催   Country:Japan  

  6. オリゴデンドロサイトへ分化誘導したグリア前駆細胞のエクソソーム放出機序オリゴデンドロサイトへ分化誘導したグリア前駆細胞のエクソソーム放出機序

    小野健治, 伊藤友香, 鈴木弘美, 澤田 誠

    第44回日本神経科学大会  2021.7  東京大学大学院医学研究科 尾藤晴彦

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    Event date: 2021.7

    Language:English   Presentation type:Poster presentation  

    Venue:神戸コンベンションセンター   Country:Japan  

  7. オリゴデンドロサイトへ分化誘導したグリア前駆細胞株から放出されるエクソソームの性質

    小野健治, 大橋和哉, 鈴木弘美, 澤田 誠

    第43回日本神経科学大会  2020.8.1  大阪大学 北澤茂

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    Event date: 2020.7 - 2020.8

    Language:English   Presentation type:Poster presentation  

    Venue:神戸   Country:Japan  

  8. ホットメルトレーザーマイクロダイセクションおよび並列LCを用いた高速LC-MSイメージングシステムの開発

    古賀裕介, 洪暎淳, 松本龍太, 鈴木弘美, 小野健治, 前田裕樹, 小河潔, 澤田 誠

    第68回日本質量分析総合討論会  2020.5.11  一般社団法人 日本質量分析学会 川﨑 英也

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    Event date: 2020.5

    Language:Japanese   Presentation type:Poster presentation  

    Venue:大阪   Country:Japan  

  9. 神経変性疾患に関連する薬剤と神経伝達物質およびL-アミノ酸のLC-MS/MS条件の最適化

    名城大学薬学部環境科学研究室発表会 

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    Event date: 2018.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名城大学薬学部   Country:Japan  

  10. Preliminary study on LC-MS/MS analysis of related drugs, nuerotransmitters, translocator protein (TSPO) ligands in brain/liver homogenates by API4000 in a single HILIC system

    Andrea Roxanne J. ANAS, Morosaki Junko, Torii Yuna, Oya Michiko, Suzuki Hiromi, Imanishi Susumu Y, Sawada Makoto, Harada Ken-ichi

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    Event date: 2018.12

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  11. LC-MS/MS analysis of neurotransmitters,translocator protein (TSPO) ligands and related drugs in a single hilic system International conference

    Andrea Roxanne J. ANAS, Morosaki Junko, Torii Yuna, Oya Michiko, SuzukiHiromi, Imanishi Susumu Y, Sawada Makoto, Harada Ken-ichi

    45th Annual convention of the Philipine Society of Biochemistry and Molecular Biology 

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    Event date: 2018.11

    Language:English   Presentation type:Oral presentation (general)  

    Venue:Grand Xing Imperial Hotel(Iloilo city, Philippine)   Country:Philippines  

  12. LMD-LC-MSによる脳内の薬物動態と神経伝達物質変化の細胞毎イメージング

    鈴木弘美、Andrea Anas, 小野健治、大石幸一、澤田 誠

    第41回日本分子生物学会年会 

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    Event date: 2018.11

    Language:Japanese   Presentation type:Poster presentation  

    Venue:パシフィコ横浜(横浜市西区みなとみらい)   Country:Japan  

  13. LC-MS/MSを用いた神経伝達物質、TSPOおよび関連薬物の同時定量

    Andrea Roxanne J. ANAS, 森崎潤子, 鳥居優奈, 大矢倫子, 鈴木弘美, 今西 進, 澤田 誠, 原田健一

    第43回日本医用マススペクトル学会年会 

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    Event date: 2018.9

    Language:English   Presentation type:Poster presentation  

    Venue:北海道大学学術交流会館   Country:Japan  

  14. Liquid chromatography optimization of pilocarpine, amino acids, neurotransmitters and related drug by API4000 based on log D

    Andrea Roxanne Jocsing ANAS, 森崎 潤子, 大矢 倫子, 鈴木 弘美, 澤田 誠, 原田 健一

    日本薬学会第138年会 

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    Event date: 2018.3

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  15. MALDI MSイメージングでの生体高分子の検出やLC-MS/MS分析でも質量イメージングを可能にする技術の確立

    鈴木弘美

    神経変性疾患のPETイメージング プロジェクトミーティング 

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    Event date: 2017.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:金山研修センター   Country:Japan  

  16. MALDI MSイメージングでの生体高分子の検出やLC-MS/MS分析でも質量イメージングを可能にする技術の確立

    鈴木弘美、Andrea Anas,大矢倫子、小野健治、大石幸一、澤田誠

    第40回日本分子生物学会年会(ConBio2017) 

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    Event date: 2017.12

    Language:Japanese   Presentation type:Poster presentation  

    Venue:神戸国際展示場   Country:Japan  

  17. 光感受性陽イオンチャネルChR2を介したNG2陽性グリア前駆細胞のオリゴデンドロサイトへの分化

    小野健治、川嶋裕人、鈴木弘美、澤田誠

    第90回日本生化学会大会(ConBio2017) 

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    Event date: 2017.12

    Language:Japanese   Presentation type:Poster presentation  

    Venue:神戸国際展示場   Country:Japan  

  18. LC-MS/MS for neural catecholamines, drugs and TSPO ligands by API4000 International conference

    Anas ARJ, Suzuki H, Imanishi SY, Harada K-1, Sawada M

    RACI(Royal Australian Chemical Institute) Centenary Cogress 

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    Event date: 2017.7

    Language:English   Presentation type:Poster presentation  

    Venue:Melbourne,Australia   Country:Australia  

  19. 光感受性イオンチャネルChRGRを介したミクログリアの機能制御

    小野健治、鈴木弘美,今野歩、石塚徹、平井宏和、八尾寛、澤田誠

    第40回日本神経科学大会 

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    Event date: 2017.7

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  20. LC-MS Imagingによる脳内での薬物動態と神経伝達物質変化の同時解析

    大矢倫子、鈴木弘美、大石幸一、小野健治、澤田誠

    第2回医薬系3部局交流シンポジウム 環境医学研究所・群馬大学生体調節研究所合同シンポジウム 

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    Event date: 2017.6

    Language:Japanese   Presentation type:Poster presentation  

    Venue:名古屋大学 野依記念学術交流館   Country:Japan  

  21. LC-MS Imagingによる脳内での薬物動態と神経伝達物質変化の同時解析

    大矢倫子、鈴木弘美、大石幸一、小野健治、澤田誠

    第65回質量分析総合討論会 

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    Event date: 2017.5

    Language:Japanese   Presentation type:Poster presentation  

    Venue:つくば国際会議場   Country:Japan  

  22. Optimization for Neural Catecholamines, its metabolites and Related Drugs in a Sigle LC-MS/MS Analysis using API4000

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    Event date: 2017.3

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  23. Optimization for Neural Catecholamines, its metabolites and Related Drugs in a Sigle LC-MS/MS Analysis using API4000

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    Event date: 2017.3

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  24. ミクログリアのサブタイプイメージング

    鈴木弘美

    神経変性疾患のPETイメージングに関する共同研究を検討するミーティング 

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    Event date: 2016.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:国立長寿研究センター   Country:Japan  

  25. 光感受性イオンチャネルChRGRを介したミクログリアの機能調節に関する解析

    小野健治、鈴木弘美、今野 歩、平井宏和、八尾 寛、澤田 誠

    第89回日本生化学会大会in 仙台 

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    Event date: 2016.9

    Language:English   Presentation type:Oral presentation (general)  

    Venue:仙台国際センター   Country:Japan  

  26. グリア前駆細胞株OS3細胞のチャネルロドプシン2を介したオリゴデンドロサイトの分化

    小野健治、山本龍生、佐橋秀紀、滝戸悠平、呉起、鈴木弘美、澤田 誠

    第39回日本神経科学会 

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    Event date: 2016.7

    Language:English   Presentation type:Poster presentation  

    Venue:パシフィコ横浜   Country:Japan  

  27. 3D質量分析イメージングを実現する前処理技術

    澤田誠、鈴木弘美、小野健治、大石幸一

    第64回日本質量分析総合討論会 

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    Event date: 2016.5

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  28. 光刺激したグリア前駆細胞株OS3ChR2細胞注入による脱髄疾患モデルマウスの運動機能改善

    小野健治、滝戸悠平、山本龍生、佐橋秀紀、鈴木弘美、澤田 誠

    第38回日本分子生物学会年会・第88回日本生化学会大会合同大会 

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    Event date: 2015.12

    Language:Japanese   Presentation type:Poster presentation  

    Venue:神戸ポートアイランド   Country:Japan  

  29. ミクログリアのサブタイプイメージング

    鈴木弘美

    先端総合イメージングセミナー2015 

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    Event date: 2015.2

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名鉄ニューグランドホテル   Country:Japan  

  30. Detection of Aβ1-40 monomer/polymers on mouse brain sections by LMD-based MS imaging

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    Event date: 2014.5

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  31. グリア前駆細胞株OS3のチャネルロドプシン2を介したオリゴデンドロサイトへの分化

    小野健治、滝戸悠平、山本龍生、佐橋秀紀,呉起、鈴木弘美、澤田誠

    第86回日本生化学会大会 

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    Event date: 2013.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:パシフィコ横浜   Country:Japan  

  32. Glutamate release from astrocyte cell-line GL261 by photo-activated channelrhodopsin-2

    Ono Kenji, Higa Madoka, Tabata Kaori, Suzuki Hiromi, Sawada Makoto

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    Event date: 2013.6

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  33. チャネルロドプシン2を導入したOS3グリア前駆細胞株における細胞分化の光制御

    小野健治、山本龍生、佐橋秀紀、鈴木弘美、澤田 誠

    第85回日本生化学会大会 

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    Event date: 2012.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡国際会議場   Country:Japan  

  34. ChR2を導入した神経系前駆細胞株OS3細胞における細胞分化の光制御

    小野 健治,山本 龍生,佐橋 秀紀,鈴木 弘美,澤田誠

    第35回日本神経科学大会 

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    Event date: 2012.9

    Language:Japanese   Presentation type:Poster presentation  

    Venue:名古屋国際会議場   Country:Japan  

  35. 活性化に伴いiNOSを発現する細胞をMRIで可視化する方法の開発

    小野健治、田畑香織、鈴木弘美、澤田誠

    第34回日本神経科学大会 

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    Event date: 2011.9

    Language:English   Presentation type:Oral presentation (general)  

    Venue:パシフィコ横浜   Country:Japan  

  36. オリゴデンドロサイトへ分化誘導したグリア前駆細胞から放出されるエクソソーム

    小野健治, 伊藤友香, 大橋和哉, 鈴木弘美, 澤田 誠

    Neuro2022(第45回日本神経科学大会、第65回日本神経化学会大会、第32回日本神経回路学会大会)  2022.7.1 

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    Event date: 2011.6 - 2022.7

    Language:Japanese   Presentation type:Poster presentation  

    Venue:沖縄   Country:Japan  

  37. 浸透圧性脱髄ラットモデルにおける脱髄病変内ミクログリアの遺伝子発現プロファイル

    鈴木陽之、椙村益久、岩間信太郎、清田敦、鈴木弘美、長崎弘、有馬寛、澤田 誠、大磯ユタカ 

    第84回日本内分泌学会学術総会 

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    Event date: 2011.4

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸国際会議場(神戸)   Country:Japan  

  38. Control of activation in ChR2-expressing astrocytes by blue light exposure

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    Event date: 2010.12

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  39. Comparative analysis of gene expression profiles of microglia from demyelinative lesions in osmotic demyelination syndrome rat model International conference

    10th International Congress of Neuroimmunology 

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    Event date: 2010.10

    Language:English   Presentation type:Poster presentation  

  40. Control of activation in ChR2-expressing astrocytes by blue light exposure

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    Event date: 2010.9

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  41. 頭の中のよい脳と悪い脳

    鈴木弘美

    名古屋大学環境医学研究所市民公開講座 

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    Event date: 2009.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  42. Protective effects of minocycline on osmotic demyelination syndrome in rats International conference

    Neuroscience 2009 

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    Event date: 2009.10

    Language:English   Presentation type:Poster presentation  

  43. Neuroprotective or neurotoxic phenotypes of activated microglia in neonatal mice in neronal injuries

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    Event date: 2009.9

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  44. Protective roles of brain-migrated immature bone marrow cells against NO-dependent neurotoxicityi n a brain injury

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    Event date: 2009.9

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  45. Minocycline prevents osmotic demyelination by inhibiting the activation of microglia in rats. International conference

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    Event date: 2009.9

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  46. SIADHモデルラットにおいてミノサイクリンは浸透圧性脱随の発症・進展を防止する

    鈴木陽之、椙村益久、岩間信太郎、鈴木弘美、有馬 寛、澤田 誠、大磯ユタカ

    第36回日本神経内分泌学会学術集会 

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    Event date: 2009.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  47. *A practical preparation of [18F]FEPPA using a protic solvent system International conference

    18th International Symposium on Radiopharmaceutical Sciences 

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    Event date: 2009.7

    Language:English   Presentation type:Poster presentation  

  48. Enhancement of glioma formation and growth by brain-migrated immature bone marrow cells

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    Event date: 2008.12

    Language:English   Presentation type:Poster presentation  

    Country:Japan  

  49. The expression of proinflammatory cytokines and neurotrophins in glia in osmotic demyelination syndrome International conference

    Society for Neuroscience 

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    Event date: 2008.11

    Language:English   Presentation type:Poster presentation  

  50. 脳損傷モデルマウスにおける脳移行性骨髄細胞の神経保護効果

    小野健治、山本奈穂、鈴木弘美、佐藤愛美、澤田 誠

    第51回神経化学会大会 

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    Event date: 2008.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  51. 脳移行性骨髄細胞の脳腫瘍形成・増殖に対する促進的関与

    小野健治、古川大記、鈴木弘美、佐藤愛美、澤田 誠

    第31回神経科学学会 

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    Event date: 2008.7

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  52. 新規抹消性ベンゾジアゼピン受容体製剤:{18F}FEPPA PETとパーキンソン病モデルラットを用いた活性化ミクログリアのイメージング

    鈴木弘美、外山宏、籏野健太郎、工藤 元、伊藤文隆、小野健治、加藤隆司、Alan Wilson,伊藤健吾、市瀬正則、澤田 誠

    第3回日本分子イメージング学会 

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    Event date: 2008.5

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  53. 浸透圧性脱髄症候群ラットッモデルにおけるグリア細胞の各種サイトカイン及び神経栄養因子の発現解析の検討

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    Event date: 2008.5

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  54. Expressionof Cytokins and Neurotrophins after acute Subarachnoid Hemorrhage. International conference

    International Stroke Conference 2008 

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    Event date: 2008.2

    Language:English   Presentation type:Oral presentation (general)  

  55. 脳損傷モデルマウスにおける脳移行性骨髄細胞の活性化と分化に関する解析

    小野健治、山本奈穂、鈴木弘美、佐藤愛美、神澤孝夫、澤田 誠

    第30回日本分子生物学会年会・第80回日本生化学会大会 

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    Event date: 2007.12

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  56. 動物PETによるラット線条体障害モデルにおけるミクログリア毒性転換の検討

    鈴木弘美、外山 宏、籏野健太郎、工藤 元、伊藤文隆、小野健治、加藤隆司、伊藤健吾、澤田 誠

    第12回グリア研究会 

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    Event date: 2007.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  57. 動物PETによるラット線条体障害モデルにおけるミクログリア毒性転換の検討

    鈴木弘美、外山宏、籏野健太郎、工藤元、伊藤文隆、小野健治、加藤隆司、伊藤健吾、澤田誠

    第16回日本バイオイメージング学会学術集会 

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    Event date: 2007.11

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  58. 脳損傷モデルマウスにおける脳移行性骨髄細胞の活性化と分化のイメージング

    小野健治、山本奈穂、鈴木弘美、神澤孝夫、澤田 誠

    第50回日本神経化学会(横浜)大会 

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    Event date: 2007.9

    Language:Japanese   Presentation type:Poster presentation  

    Country:Japan  

  59. 動物PETによるラット線条体障害モデルにおけるミクログリア毒性転換の検討

    伊藤文隆、工藤 元、外山 宏、鈴木弘美、籏野健太郎、加藤隆司、片田和広、市瀬正則、澤田 誠、伊藤健吾

    第2回日本分子イメージング学会総会・学術集会 

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    Event date: 2007.6

    Language:Japanese   Presentation type:Poster presentation  

  60. Imaging of activated microglia in brain injury

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    Event date: 2006.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  61. Activated microglia affect the nigro-striatal dopamine neurons differently in neonatal and aged mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. International conference

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB Gongress 

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    Event date: 2006.6

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  62. 1.5T MRIによる定位的ラット脳線条体撮像ー定位脳固定具を用いない撮像法の開発

    伊藤文隆, 工藤 元, 外山 宏, 鈴木弘美, 旗野健太郎, 中根正人, 大橋正夫, 加藤隆司, 片田和広, 市瀬正則, 澤田 誠, 伊藤健吾

    日本分子イメージング学会設立総会および第1回学術集会 

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    Event date: 2006.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  63. 末梢性ベンゾジアゼピン受容体製剤11C-CB148と11C-PK11195の比較―動物PETによる検討

    関亦克彦,籏野健太郎,外山 宏,鈴木弘美,加藤隆司,片田和廣,澤田 誠, 伊藤健吾

    第45回日本核医学会総会 

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    Event date: 2005.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  64. 活性型ミクログリアのIn Vivoイメージング

    鈴木弘美, 外山 宏, 工藤 元, 籏野健太郎, 関亦克彦, 小野健治, 中根正人, 加藤隆司, 伊藤健吾, 澤田 誠

    第14回日本バイオイメージング学会学術集会 

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    Event date: 2005.10

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  65. HIV-Nefを導入したミクログリア細胞による神経細胞機能障害

    澤田 誠,三井健一,鈴木弘美,小野健治,Karl-Heinz Krause,鈴木和男

    第16回日本生体防御学術集会 

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    Event date: 2005.8

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  66. 末梢性ベンゾジアゼピン受容体製剤11C-CB148と11C-PK11195の比較―動物PETによる検討

    工藤元,関亦克彦,籏野健太郎、外山宏,鈴木弘美,加藤隆司,片田和廣,澤田 誠,伊藤健吾

    核医学会中部地方会 

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    Event date: 2005.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  67. 活性型ミクログリアのIn Vivoイメージング

    鈴木弘美, 外山宏, 工藤元, 旗野健太郎, 関亦克彦,小野健治, 加藤隆司, 伊藤健吾,澤田 誠

    第9回ニューロイメージングカンファランス 

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    Event date: 2005.2

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  68. ChR2を導入した神経系前駆細胞株OS3細胞における細胞分化の光制御 International conference

    小野 健治, 山本 龍生, 佐橋 秀紀, 鈴木 弘美, 澤田誠

    第35回日本神経科学大会  2012.9.18 

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:名古屋国際会議場  

  69. 3D質量分析イメージングを実現する前処理技術 International conference

    澤田誠, 鈴木弘美, 小野健治, 大石幸一

    第64回日本質量分析総合討論会  2016.5.18 

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    Language:Japanese   Presentation type:Poster presentation  

  70. LC-MS/MS for neural catecholamines, drugs and TSPO ligands by API4000

    Anas ARJ, Suzuki H, Imanishi SY, Harada K, Sawada M

    RACI(Royal Australian Chemical Institute) Centenary Cogress  2017.7.23 

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    Language:English   Presentation type:Poster presentation  

    Venue:Melbourne,Australia  

  71. LC-MS/MS analysis of neurotransmitters,translocator protein (TSPO) ligands and related drugs in a single hilic system

    Andrea Roxanne, J. ANAS, Morosaki Junko, Torii Yuna, Oya Michiko, SuzukiHiromi, Imanishi Susumu Y, Sawada Makoto, Harada Ken-ichi

    45th Annual convention of the Philipine Society of Biochemistry and Molecular Biology  2018.11.27 

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:Grand Xing Imperial Hotel(Iloilo city, Philippine)  

  72. 光刺激したグリア前駆細胞株OS3ChR2細胞注入による脱髄疾患モデルマウスの運動機能改善 International conference

    小野健治, 滝戸悠平, 山本龍生, 佐橋秀紀, 鈴木弘美, 澤田 誠

    第38回日本分子生物学会年会・第88回日本生化学会大会合同大会  2015.12.1 

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:神戸ポートアイランド  

  73. ミクログリアのサブタイプイメージング International conference

    鈴木弘美

    神経変性疾患のPETイメージングに関する共同研究を検討するミーティング  2016.12.16 

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    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:国立長寿研究センター  

  74. ミクログリアのサブタイプイメージング International conference

    鈴木弘美

    先端総合イメージングセミナー2015  2015.2.21 

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    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名鉄ニューグランドホテル  

  75. チャネルロドプシン2を導入したOS3グリア前駆細胞株における細胞分化の光制御 International conference

    小野健治, 山本龍生, 佐橋秀紀, 鈴木弘美, 澤田 誠

    第85回日本生化学会大会  2012.12.14 

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    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡国際会議場  

  76. グリア前駆細胞株OS3細胞のチャネルロドプシン2を介したオリゴデンドロサイトの分化 International conference

    小野健治, 山本龍生, 佐橋秀紀, 滝戸悠平, 呉起, 鈴木弘美, 澤田 誠

    第39回日本神経科学会  2016.7.20 

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    Language:English   Presentation type:Poster presentation  

    Venue:パシフィコ横浜  

  77. グリア前駆細胞株OS3のチャネルロドプシン2を介したオリゴデンドロサイトへの分化 International conference

    小野健治, 滝戸悠平, 山本龍生, 佐橋秀紀, 呉起, 鈴木弘美, 澤田誠

    第86回日本生化学会大会  2013.9.11 

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    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:パシフィコ横浜  

  78. 光感受性イオンチャネルChRGRを介したミクログリアの機能制御 International conference

    小野健治, 鈴木弘美, 今野歩, 石塚徹, 平井宏和, 八尾寛, 澤田誠

    第40回日本神経科学大会  2017.7.20 

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    Language:English   Presentation type:Poster presentation  

  79. 神経変性疾患に関連する薬剤と神経伝達物質およびL-アミノ酸のLC-MS/MS条件の最適化 International conference

    Torii Yuna, Andrea Roxanne, J. ANAS, Morosaki Junko, Oya Michiko, Suzuki Hiromi, Imanishi Susumu Y, Sawada Makoto, Harada Ken-ichi

    名城大学薬学部環境科学研究室発表会  2018.12.8 

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    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名城大学薬学部  

  80. 浸透圧性脱髄ラットモデルにおける脱髄病変内ミクログリアの遺伝子発現プロファイル International conference

    鈴木陽之, 椙村益久, 岩間信太郎, 清田敦, 鈴木弘美, 長崎弘, 有馬寛, 澤田 誠, 大磯ユタカ

    第84回日本内分泌学会学術総会  2011.4.21 

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    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸国際会議場(神戸)  

  81. 活性化に伴いiNOSを発現する細胞をMRIで可視化する方法の開発 International conference

    小野健治, 田畑香織, 鈴木弘美, 澤田誠

    第34回日本神経科学大会  2011.9.14 

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:パシフィコ横浜  

  82. Detection of Aβ1-40 monomer/polymers on mouse brain sections by LMD-based MS imaging International conference

    2014.5.22 

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    Language:Japanese   Presentation type:Poster presentation  

  83. 光感受性陽イオンチャネルChR2を介したNG2陽性グリア前駆細胞のオリゴデンドロサイトへの分化 International conference

    小野健治, 川嶋裕人, 鈴木弘美, 澤田誠

    第90回日本生化学会大会(ConBio2017)  2017.12.6 

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:神戸国際展示場  

  84. 光感受性イオンチャネルChRGRを介したミクログリアの機能調節に関する解析 International conference

    小野健治, 鈴木弘美, 今野 歩, 平井宏和, 八尾 寛, 澤田 誠

    第89回日本生化学会大会in 仙台  2016.9.25 

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:仙台国際センター  

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Research Project for Joint Research, Competitive Funding, etc. 10

  1. 神経変性疾患の創薬標的たるマイクログリア特異的発現分子のPETイメージングの開発

    Grant number:18H02776  2018.4 - 2021.3

    国立研究開発法人 国立長寿医療研究センター  基盤研究 (B) 

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    Authorship:Coinvestigator(s)  Grant type:Competitive

    Grant amount:\150

  2. シグナルペプチド:細胞外微粒子機能の新規マーカー

    2017.10 - 2023.3

    CREST 

    鈴木弘美

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    Authorship:Collaborating Investigator(s) (not designated on Grant-in-Aid)  Grant type:Competitive

    Grant amount:\191975680 ( Direct Cost: \185697499 、 Indirect Cost:\6298719 )

  3. Role of diabetes and inflammation on microglial cell biology and transformation International coauthorship

    2020.10 - 2021.10

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    Authorship:Coinvestigator(s)  Grant type:Collaborative (industry/university)

    Grant amount:\24670482 ( Direct Cost: \24670482 )

  4. 新規な脳腫瘍診断マーカー遺伝子の探索

    2023.4

    医療法人 今井病院 今井文博  共同研究費 

    鈴木弘美

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    Authorship:Principal investigator  Grant type:Collaborative (industry/university)

    Grant amount:\460000 ( Direct Cost: \460000 )

  5. エクソソームの大量調製条件の検討

    2023.4 - 2027.3

    共同研究費 

    鈴木弘美

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1300000 ( Direct Cost: \1200000 、 Indirect Cost:\100000 )

  6. 中枢作用のある薬剤の単一細胞質量分析による動態解析

    2019.4 - 2022.3

    国内共同研究 

    鈴木弘美

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    Authorship:Coinvestigator(s)  Grant type:Collaborative (industry/university)

    Grant amount:\1729700 ( Direct Cost: \1729700 )

  7. LMD技術に関する研究

    2018.4 - 2020.10

    国内共同研究 

    鈴木弘美

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    Authorship:Coinvestigator(s)  Grant type:Collaborative (industry/university)

    Grant amount:\882320

  8. 標的化技術の評価にかかる共同研究

    2010.6 - 2011.3

    国内共同研究 

  9. 脳疾患に対する新規機能抗体の開発とその応用

    2010.6

    国内共同研究 

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    株化ミクログリアを用いて細胞膜上の生体情報授受に関わる受容体に対する抗体を取得し、新規の機能抗体の開発と応用を目指す。

  10. 脳標的化薬物送達を目的とするシャトルステーション型のステントの開発

    2009.8 - 2010.3

    A-step 

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    Grant type:Competitive

    現在、気道・胆管・血管などの狭窄部位挿入し、内側から広げ支える治療器具として使用されている合金製ステントを、埋め込み型の薬剤除去システム【シャトルステーション型ステント】として改良し実用化を目指すものである。提案期間には模擬生体内条件から小動物血管を用いた利用効率を検討する。

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KAKENHI (Grants-in-Aid for Scientific Research) 1

  1. 神経変性疾患の創薬標的たるマイクログリア特異的発現分子のPETイメージングの開発

    Grant number:18H02776  2018.4 - 2021.3

    国立研究開発法人 国立長寿医療研究センター   基盤研究 (B) 

    木村泰之

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    Authorship:Coinvestigator(s)  Grant type:Competitive

    Grant amount:\500000 ( Direct Cost: \500000 、 Indirect Cost:\30000 )

Industrial property rights 7

  1. 質量分析方法

    東海国立大学機構,JSR,島津製作所

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    Applicant:澤田 誠, 小野健治, 鈴木弘美, 王 勇, 緒方是嗣, 村田 匡

    Application no:PCT/JP2021/044239  Date applied:2021.12

    Announcement no:WO2022/131000  Date announced:2022.6

    Country of applicant:Domestic , Foreign country   Country of acquisition:Domestic , Foreign country

  2. レーザマイクロダイセクション装置

    澤田 誠, 鈴木弘美, 小野健治, 洪 暎淳

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    Applicant:東海国立大学機構, 島津製作所

    Application no:PCT/JP2020/011793  Date applied:2020.3

    Announcement no:WO 2021/186577  Date announced:2021.9

    Country of applicant:Domestic , Foreign country   Country of acquisition:Domestic , Foreign country

  3. 多価結合手を有し代謝安定性が向上した脳移行性ポリペプチド

    中條 智洋, 原 啓高, 山本 一匡, 鈴木 弘美, 澤田 誠, 須原 哲也, 樋口 真人, 原田平 輝志, 季 斌

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    Applicant:プロテウス・サイエンス株式会社、国立放射線科学研究所

    Application no:特願2009-502538  Date applied:2008.2

    Publication no:WO 2008/108242 A1  Date published:2008.9

    Patent/Registration no:特許第5250849号  Date registered:2013.4 

    Country of applicant:Domestic , Foreign country   Country of acquisition:Domestic , Foreign country

    J-GLOBAL

  4. 金属コロイド粒子を含有する脳神経細胞内移行用キャリア

    澤田 誠, 鈴木 弘美

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    Applicant:株式会社ティッシュターゲティングジャパン

    Application no:JP2005001761  Date applied:2005.2

    Announcement no:WO 2006/013650 A1  Date announced:2006.2

    Publication no:WO2006-013650  Date published:2006.2

    Country of applicant:Domestic , Foreign country   Country of acquisition:Domestic , Foreign country

    J-GLOBAL

  5. PESI-MSでのイオン化の効率を上げる手法

    澤田 誠, 小野健治, 鈴木弘美, 王 勇, 緒方是嗣, 村田 匡

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    Applicant:東海国立大学機構, JSR, 島津製作所

    Application no:WUS0001418 

  6. 多価結合手を有し代謝安定性が向上した脳移行性ポリペプチド

    中條智洋、原啓高、山本一匡、鈴木弘美、澤田誠、須原哲也、樋口真人、原田平輝志、季斌

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    Application no:特願2007-054260  Date applied:2007.3

    Country of applicant:Domestic  

  7. 金属コロイド粒子を含有する脳神経細胞内移行用キャリア

    澤田誠, 鈴木弘美

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    Application no:PCT/JP2005/001761  Date applied:2005.2

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Teaching Experience (On-campus) 11

  1. ベーシックトレーニング

    2023

     詳細を見る

    顕微鏡下で組織サンプルの画像取得後、画像データを基に病態由来の細胞を同定・解析し、座標再現機能を装着したマイクロディセクション顕微鏡を用いて半自動操作により採取・分離する技術について実践します。さらに、分取細胞の質量分析を行い、分析結果を元の画像に重ねてLC-MS/MALDI 質量分析イメージングにチャレンジします。

  2. 基礎医学セミナー

    2022

  3. ベーシックトレーニング

    2022

  4. ベーシックトレーニング

    2021

  5. 基礎医学セミナー

    2021

  6. ベーシックトレーニング

    2020

  7. 基礎医学セミナー

    2020

  8. ベーシックトレーニング

    2019

  9. 基礎医学セミナー

    2019

  10. 基礎医学セミナー

    2018

  11. ベーシックトレーニング

    2010

▼display all

Teaching Experience (Off-campus) 4

  1. 大学院講義

    2019.4 - 2020.3 Fujita Health University)

  2. 2018.4 - 2019.3 Fujita Health University)

  3. ベーシックトレーニング

    Nagoya University)

  4. ベーシックトレーニング

    Nagoya University)