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Targeted deletion of Atg5 in intestinal epithelial cells promotes dextran sodium sulfate-induced colitis.
http://hdl.handle.net/10422/00012938
http://hdl.handle.net/10422/0001293882358c7a-cf6c-46db-98e3-e8fbc0f5d84f
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
jcbn.20-90 (1.4 MB)
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This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License.
https://creativecommons.org/licenses/by-nc-nd/4.0/ |
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2021-04-07 | |||||
| タイトル | ||||||
| タイトル | Targeted deletion of Atg5 in intestinal epithelial cells promotes dextran sodium sulfate-induced colitis. | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | autophagy | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | IRE1α | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | IBD | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
NISHINO, Kyohei
× NISHINO, Kyohei× NISHIDA, Atsushi× INATOMI, Osamu× IMAI, Takayuki× KUME, Shinji× KAWAHARA, Masahiro× MAEGAWA, Hiroshi× ANDOH, Akira |
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| 著者別名 |
西野, 恭平
× 西野, 恭平× 西田, 淳史× 稲富, 理× 今井, 隆行× 久米, 真司× 河原, 真大× 前川, 聡× 安藤, 朗 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Autophagy-associated genes have been identified as susceptible loci for inflammatory bowel disease. We investigated the role of a core autophagy factor, Atg5, in the development of dextran sodium sulfate (DSS)-induced colitis. Intestinal epithelial cell (IEC)-specific Atg5 gene deficient mice (Atg5ΔIEC mice) were generated by cross of Atg5-floxed mice (Atg5fl/fl) with transgenic mice expressing Cre-recombinase driven by the villin promotor. Mice were given three cycles of 1.5% DSS in drinking water for 5 days and regular water for 14 days over a 60-day period. The dysfunction of autophagy characterized by a marked accumulation of p62 protein, a substrate for autophagy degradation, was detected in epithelial cells in the non-inflamed and inflamed mucosa of inflammatory bowel disease patients. DSS-colitis was exacerbated in Atg5ΔIEC mice compared to control Atg5fl/fl mice. Phosphorylation of inositol-requiring transmembrane kinase/endonuclease1α (IRE1α), a sensor for endoplasmic reticulum stress, and c-Jun N-terminal kinase, a downstream target of IRE1α, were significantly enhanced in IECs in DSS-treated Atg5ΔIEC mice. Accumulation of phosphorylated IRE1α was enhanced by the treatment with chloroquine, an autophagy inhibitor. Apoptotic IECs were more abundant in DSS-treated Atg5ΔIEC mice. These findings suggest that Atg5 suppresses endoplasmic reticulum stress-induced apoptosis of IECs via the degradation of excess p-IRE1α. | |||||
| 書誌情報 |
en : Journal of Clinical Biochemistry and Nutrition 巻 68, 号 2, p. 156-163, 発行日 2021 |
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| 出版者 | ||||||
| 出版者 | 一般社団法人 日本酸化ストレス学会 | |||||
| 別言語の出版者 | ||||||
| 出版者 | SOCIETY FOR FREE RADICAL RESEARCH JAPAN | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0912-0009 | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.3164/jcbn.20-90 | |||||
| 関連名称 | 10.3164/jcbn.20-90 | |||||
| 権利 | ||||||
| 権利情報 | © 2021 JCBN | |||||
| フォーマット | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | ||||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
| NAID | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | NAID | |||||
| 関連識別子 | 130007993417 | |||||
| 資源タイプ | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Journal Article | |||||
