Abrogated Caveolin-1 expression via histone modification enzyme Setdb2 regulates brain edema in a mouse model of influenza-associated encephalopathy.

• Material Type: 博士論文
• Title: Abrogated Caveolin-1 expression via histone modification enzyme Setdb2 regulates brain edema in a mouse model of influenza-associated encephalopathy.
• Author/Editor: Imakita, Natsuko; Kitabatake, Masahiro; Ouji-Sageshima, Noriko; Hara, Atsushi; Morita-Takemura, Shoko; Kasahara, Kei; Matsukawa, Akihiro; Wanaka, Akio; Mikasa, Keiichi; Ito, Toshihiro
• Author Heading: Imakita, Natsuko; Kitabatake, Masahiro; Ouji-Sageshima, Noriko; Hara, Atsushi; Morita-Takemura, Shoko; Kasahara, Kei; Matsukawa, Akihiro; Wanaka, Akio; Mikasa, Keiichi; Ito, Toshihiro
• Publication, Distribution, etc.: Springer Nature Publishing AG
• Publication Date: 2019-01-22
• Publication Date (W3CDTF): 2019-01-22
• Alternative Title: ヒストン修飾酵素Setdb2を介したCaveolin-1はインフルエンザ脳症マウスモデルにおける脳浮腫を制御する
• Periodical title: Scientific reports
• No. or year of volume/issue: 9 1
• Volume: 9
• Issue: 1
• Pages: Article No.284-
• ISSN (Periodical Title): ISSN : 2045-2322
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2019-03-15
• Dissertation Number: 甲第706号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Target Audience: 一般
• Note (General): type:Thesis; Influenza-associated encephalopathy (IAE) is a serious complication that can follow influenza virus infection. Once a cytokine storm is induced during influenza virus infection, tight junction protein disruption occurs, which consequently leads to blood-brain barrier (BBB) breakdown. However, the details of IAE pathogenesis are not well understood. Here, we established a murine IAE model by administration of lipopolysaccharide following influenza virus infection. Brains from IAE model mice had significantly higher expression of type I interferons and inflammatory cytokines. In addition, the expression of Caveolin-1, one of the key proteins that correlate with protection of the BBB, was significantly lower in brains from the IAE group compared with the control group. We also found that, among 84 different histone modification enzymes, only SET domain bifurcated 2 (Setdb2), one of the histone methyltransferases that methylates the lysine 9 of histone H3, showed significantly higher expression in the IAE group compared with the control group. Furthermore, chromatin immunoprecipitation revealed that methylation of histone H3 lysine 9 was correlated with repression of the Caveolin-1 promoter region. These studies identify Caveolin-1 as a key regulator of BBB permeability in IAE and reveal that it acts through histone modification induced by Setdb2.; 博士（医学）・甲第706号・平成31年3月15日; © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.; © 2018 Springer Nature Publishing AG; identifier:Scientific reports Vol.9 No.1 Article No.284 (2019 Jan); identifier:20452322; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3554; identifier:Scientific reports, 9(1): Article No.284
• Source: fulltext; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3554/1/01%e7%94%b2706%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3554/2/02%e7%94%b2706%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3554/3/03%e7%94%b2706%e6%9c%ac%e6%96%87.pdf
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.1038/s41598-018-36489-8
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU