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Published Papers 【 display / non-display 】

• 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 )   2020.06 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• 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   2019.10 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• 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     2019.02 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

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• 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   2018.06 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

  　View Summary

  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.

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• 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 )   2018.03 [ Peer Review Accepted ]

  Type of publication: Research paper (scientific journal)

  　View Summary

  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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Grant-in-Aid for Scientific Research 【 display / non-display 】

Grant-in-Aid for Scientific Research 【 display / non-display 】

• Grant-in-Aid for Scientific Research(C)

  Project Year: 2019.04  -  2022.03 

  Direct: 3,300,000 (YEN)  Overheads: 990,000 (YEN)  Total: 4,290,000 (YEN)

• Grant-in-Aid for Scientific Research(C)

  Project Year: 2014.04  -  2017.03 

  Direct: 3,800,000 (YEN)  Overheads: 1,140,000 (YEN)  Total: 4,940,000 (YEN)

• Grant-in-Aid for Scientific Research on Innovative Areas

  Project Year: 2012.06  -  2017.03 

• Grant-in-Aid for Young Scientists(B)

  Project Year: 2006.04  -  2008.03 

  Direct: 3,500,000 (YEN)  Total: 3,500,000 (YEN)