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Original Research—Basic|Articles in Press

Deletion of miR-150 prevents spontaneous T cell proliferation and the development of colitis

  • Author Footnotes
    ∗ S.I. and M.S. contributed equally to this study.
    Sayaka Ishihara
    Footnotes
    ∗ S.I. and M.S. contributed equally to this study.
    Affiliations
    Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, minamiku, Sagamihara, Kanagawa 252-0344, Japan

    Department of Innovative Medical Science, School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan
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  • Author Footnotes
    ∗ S.I. and M.S. contributed equally to this study.
    Masashi Sato
    Footnotes
    ∗ S.I. and M.S. contributed equally to this study.
    Affiliations
    Department of Immunology, School of Medicine, Kitasato University, 1-15-1 Kitasato, minamiku, Sagamihara, Kanagawa 252-0344, Japan
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  • Haruka Miyazaki
    Affiliations
    Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, minamiku, Sagamihara, Kanagawa 252-0344, Japan
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  • Haruka Saito
    Affiliations
    Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, minamiku, Sagamihara, Kanagawa 252-0344, Japan
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  • Tsuyoshi Sato
    Affiliations
    Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, minamiku, Sagamihara, Kanagawa 252-0344, Japan
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  • Noriyuki Fujikado
    Affiliations
    Discovery Immunology, Ferring Research Institute, Ferring Pharmaceuticals
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  • Satoshi Sawai
    Affiliations
    Department of Basic Science, Graduate School of Arts and Sciences, University of Tokyo, Tokyo 153-8902, Japan
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  • Ai Kotani
    Affiliations
    Department of Innovative Medical Science, School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan

    Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan
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  • Koko Katagiri
    Correspondence
    Correspondence: Koko Katagiri, Department of Innovative Medical Science, School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan,
    Affiliations
    Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, minamiku, Sagamihara, Kanagawa 252-0344, Japan

    Department of Basic Science, Graduate School of Arts and Sciences, University of Tokyo, Tokyo 153-8902, Japan

    Department of Innovative Medical Science, School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan
    Search for articles by this author
  • Author Footnotes
    ∗ S.I. and M.S. contributed equally to this study.
Open AccessPublished:February 04, 2023DOI:https://doi.org/10.1016/j.gastha.2023.01.021
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      Abstract

      Background & Aims

      To examine the roles of microRNAs in the development of colitis, we conducted the RNA-sequencing studies using RNA derived from normal and colitogenic CD4+ T cells. Colitogenic CD4+ T cells demonstrated the increased expression of miR-150. We focused on the involvement of miR-150 in the colitis.

      Methods

      We crossed miR-150 knockout (KO) mice and T-cell specific Rap1KO mice, which is colitis model mice and spontaneously develop the colitis with tubular adenomas in microbiota-dependent manner.

      Results

      MiR-150 silencing completely inhibited the expansion of pathogenic Th17 cells and the development of colitis.

      Conclusion

      MiR-150 is a potential therapeutic target of inflammatory bowel diseases.

      Key words

      Abbreviation:

      Th (T helper), RORγt (retinoic acid receptor-related orphan receptor gamma), TCR (T-cell receptor)