大野 真治 (オオノ シンジ)

Ohno Shinji

写真a

職名

教授

科研費研究者番号

50419529

現在の所属組織 【 表示 / 非表示

  • 専任   琉球大学   医学研究科   教授  

出身大学 【 表示 / 非表示

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    1999年03月

    九州大学   医学部   卒業

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    2005年03月

    九州大学大学院   医学研究府   卒業

出身大学院 【 表示 / 非表示

  •  
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    1999年03月

    九州大学  医学部  博士課程  修了

  •  
    -
    2005年03月

    九州大学大学院  医学研究府  博士課程  修了

取得学位 【 表示 / 非表示

  • 九州大学 -  博士(医学)  医学

職歴 【 表示 / 非表示

  • 2005年04月
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    2006年03月

       

  • 2006年04月
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    2007年01月

       

  • 2007年02月
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    2012年09月

       

  • 2012年10月
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    2016年03月

       

  • 2016年04月
     
     

       

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所属学会・委員会 【 表示 / 非表示

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    日本ウイルス学会

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    日本免疫学会

取得資格 【 表示 / 非表示

  • 医師

論文 【 表示 / 非表示

  • Lysosome-Associated Membrane Proteins Support the Furin-Mediated Processing of the Mumps Virus Fusion Protein.

    Ueo A, Kubota M, Shirogane Y, Ohno S, Hashiguchi T, Yanagi Y

    Journal of virology   94 ( 12 )   2020年06月 [ 査読有り ]

    掲載種別: 研究論文(学術雑誌)

  • A comparative epigenome analysis of gammaherpesviruses suggests cis-acting sequence features as critical mediators of rapid polycomb recruitment.

    Günther T, Fröhlich J, Herrde C, Ohno S, Burkhardt L, Adler H, Grundhoff A

    PLoS pathogens   15 ( 10 ) e1007838   2019年10月 [ 査読有り ]

    掲載種別: 研究論文(学術雑誌)

  • Both type I and type III interferons are required to restrict measles virus growth in lung epithelial cells.

    Taniguchi M, Yanagi Y, Ohno S

    Archives of virology     2019年02月 [ 査読有り ]

    掲載種別: 研究論文(学術雑誌)

  • S100a4 is secreted by alternatively activated alveolar macrophages and promotes activation of lung fibroblasts in pulmonary fibrosis

    Wei Zhang, Shinji Ohno, Beatrix Steer, Stephan Klee, Claudia A. Staab-Weijnitz, Darcy Wagner, Mareike Lehmann, Tobias Stoeger, Melanie Königshoff, Heiko Adler

    Frontiers in Immunology ( Frontiers Media S.A. )  9   1216   2018年06月 [ 査読有り ]

    掲載種別: 研究論文(学術雑誌)

     概要を見る

    Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease, characterized by damage of lung epithelial cells, excessive deposition of extracellular matrix in the lung interstitium, and enhanced activation and proliferation of fibroblasts. S100a4, also termed FSP-1 (fibroblast-specific protein-1), was previously considered as a marker of fibroblasts but recent findings in renal and liver fibrosis indicated that M2 macrophages are an important cellular source of S100a4. Thus, we hypothesized that also in pulmonary fibrosis, M2 macrophages produce and secrete S100a4, and that secreted S100a4 induces the proliferation and activation of fibroblasts. To prove this hypothesis, we comprehensively characterized two established mouse models of lung fibrosis: infection of IFN-γR-/- mice with MHV-68 and intratracheal application of bleomycin to C57BL/6 mice. We further provide in vitro data using primary macrophages and fibroblasts to investigate the mechanism by which S100A4 exerts its effects. Finally, we inhibit S100a4 in vivo in the bleomycin-induced lung fibrosis model by treatment with niclosamide. Our data suggest that S100a4 is produced and secreted by M2 polarized alveolar macrophages and enhances the proliferation and activation of lung fibroblasts. Inhibition of S100a4 might represent a potential therapeutic strategy for pulmonary fibrosis.

  • Cell-to-cell measles virus spread between human neurons is dependent on hemagglutinin and hyperfusogenic fusion protein

    Yuma Sato, Shumpei Watanabe, Yoshinari Fukuda, Takao Hashiguchi, Yusuke Yanagi, Shinji Ohno

    Journal of Virology ( American Society for Microbiology )  92 ( 6 )   2018年03月 [ 査読有り ]

    掲載種別: 研究論文(学術雑誌)

     概要を見る

    Measles virus (MV) usually causes acute infection but in rare cases persists in the brain, resulting in subacute sclerosing panencephalitis (SSPE). Since human neurons, an important target affected in the disease, do not express the known MV receptors (signaling lymphocyte activation molecule [SLAM] and nectin 4), how MV infects neurons and spreads between them is unknown. Recent studies have shown that many virus strains isolated from SSPE patients possess substitutions in the extracellular domain of the fusion (F) protein which confer enhanced fusion activity. Hyperfusogenic viruses with such mutations, unlike the wild-type MV, can induce cell-cell fusion even in SLAM- and nectin 4-negative cells and spread efficiently in human primary neurons and the brains of animal models. We show here that a hyperfusogenic mutant MV, IC323-F(T461I)-EGFP (IC323 with a fusionenhancing T461I substitution in the F protein and expressing enhanced green fluorescent protein), but not the wild-type MV, spreads in differentiated NT2 cells, a widely used human neuron model. Confocal time-lapse imaging revealed the cell-to-cell spread of IC323-F(T461I)-EGFP between NT2 neurons without syncytium formation. The production of virus particles was strongly suppressed in NT2 neurons, also supporting cell-to-cell viral transmission. The spread of IC323- F(T461I)-EGFP was inhibited by a fusion inhibitor peptide as well as by some but not all of the anti-hemagglutinin antibodies which neutralize SLAM- or nectin-4- dependent MV infection, suggesting the presence of a distinct neuronal receptor. Our results indicate that MV spreads in a cell-to-cell manner between human neurons without causing syncytium formation and that the spread is dependent on the hyperfusogenic F protein, the hemagglutinin, and the putative neuronal receptor for MV.

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科研費獲得情報 【 表示 / 非表示

  • 宮古島のHHV8にみられる遺伝子変異の意義

    基盤研究(C)

    課題番号: 19K07669

    研究期間: 2019年04月  -  2022年03月 

    直接経費: 3,300,000(円)  間接経費: 990,000(円)  金額合計: 4,290,000(円)

  • ヘルペスウイルスの遺伝子発現スイッチ機構の解明

    基盤研究(C)

    課題番号: 26460558

    研究期間: 2014年04月  -  2017年03月 

    直接経費: 3,800,000(円)  間接経費: 1,140,000(円)  金額合計: 4,940,000(円)

  • ウイルスの宿主細胞選択における攻防

    新学術領域研究

    課題番号: 24115005

    研究期間: 2012年06月  -  2017年03月 

    代表者: 柳雄介 

  • CD150遺伝子改変マウスを用いたSSPEの病態の解明

    若手研究(B)

    課題番号: 18790324

    研究期間: 2006年04月  -  2008年03月 

    直接経費: 3,500,000(円)  金額合計: 3,500,000(円)