Faculty Profiles - SUZUKI, Hiromi

Papers - SUZUKI, Hiromi

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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

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

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

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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PubMed

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

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

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

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

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

Language：English Publishing type：Research paper (scientific journal) Publisher：WILEY-V C H VERLAG GMBH

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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PubMed

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

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

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

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

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER IRELAND LTD

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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PubMed

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

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

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

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

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

Web of Science

PubMed

Comparison of the neurological sequelae after rapid correction of hyponatremia between by vasopressin receptor antagonist mozavaptan (OPC-31260) and by hypertonic saline in rats Invited Reviewed

Suzuki, H; Sugimura, Y; Iwama, S; Nagasaki, H; Arima, H; Oiso, Y

ENDOCRINE JOURNAL Vol. 57 page： S531 - S531 2010.3

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

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

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

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

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

Hirohide Sawada, Hiromi Suzuki, Toshiharu Nagatsu, Makoto Sawada

NEURODEGENERATIVE DISEASES Vol. 7 ( 1-3 ) page： 64 - 67 2010

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

Activated microglia play important roles in the inflammatory process and progression in Parkinson's disease. These cells produce various cytokines, nitric oxide, and neurotrophins, which are pleiotropic in their action, i.e., neuroprotective or neurotoxic. In an in vivo study on a mouse model with nigrostriatal lesions produced by the administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), microglia activated by systemic lipopolysaccharide (LPS) were neurotoxic toward dopamine neurons in aged mice, but unexpectedly, neuroprotective in neonatal mice. In contrast to microglia in the MPTP model, LPS-activated microglia in neonatal mice in a model made by the stereotaxic injection of ethanol into the striatum were neurotoxic, and systemic LPS administration in the ethanol-injury model caused marked increases both in the volume of necrotic lesions and in the number of degenerative neurons in the striatum. Thus, activated microglia in the neonatal mouse brain play either a neuroprotective or neurotoxic role depending on the type of brain injury. Copyright (C) 2010 S. Karger AG, Basel

DOI： 10.1159/000285508

Web of Science

PubMed

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Papers - SUZUKI, Hiromi