Faculty Profiles - SUZUKI, Hiromi

Papers - SUZUKI, Hiromi

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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

Isolation of Microglia Subpopulations Invited Reviewed

Sawada, M; Suzuki, H

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

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

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

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

Neuroprotective or neurotoxic phenotypes of activated microglia in neonatal mice in neuronal injuries Invited Reviewed

Hirohide Sawada, Hiromi Suzuki, Toshiharu Nagatsu, Makoto Sawada

NEUROSCIENCE RESEARCH Vol. 65 page： S118 - S118 2009

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

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

Language：English Publishing type：Research paper (scientific journal) Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE

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

Web of Science

PubMed

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

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

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

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

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

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

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

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

Language：English Publishing type：Research paper (scientific journal) Publisher：WILEY-LISS

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

Web of Science

PubMed

J-GLOBAL

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

[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

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

Valentino Laquintana, Nunzio Denora, Angela Lopedota, Hiromi Suzuki, Makoto Sawada, Mariangela Serra, Giovanni Biggio, Andrea Latrofa, Giuseppe Trapani, Gaetano Liso

BIOCONJUGATE CHEMISTRY Vol. 18 ( 5 ) page： 1397 - 1407 2007

Language：English Publishing type：Research paper (scientific journal) Publisher：AMER CHEMICAL SOC

The aim of this work was to develop new fluorescent probes for the localization and function of the peripheral benzodiazepine receptor (PBR). This receptor is primarily expressed on the mitochondria, and it is overexpressed in a variety of different states including glioma, breast cancer, Alzeheimer's disease, and activated microglia. For the mentioned purpose, imidazopyridine and imidazopyrimidine compounds 5-20 were synthesized, and their affinity for PBR was determined. Although some intrinsically fluorescent imidazopyrimidine compounds 12-20 possess good binding affinity, they cannot be used for visualizing PBR due to their unfavorable fluorescence characteristics. Among the imidazopyridine-7-nitrofurazan conjugates 5-11, compound 10 was the most active, and it was found to stain live Ra2 microglial cells effectively. An in vivo biodistribution study carried out on compound 10 showed that this imidazopyridine derivative, injected in the carotid artery, is able to penetrate to liver parenchyma, whereas fluorescein isothiocyanate labeled dextran (FITC-dextran), used as a control dye, hardly penetrated from blood vessels to tissues. On the other hand, as for the distribution to brain, the patterns of staining with 10 and FITC-dextran are similar, indicating that both of them hardly penetrate into the brain because of the existence of the blood-brain barrier. The obtained results indicate that compound 10 represents a new useful fluorescent probe for visualization of activated microglia and PBR.

DOI： 10.1021/bc060393c

Web of Science

PubMed

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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Papers - SUZUKI, Hiromi