Conditional Deletion of Smad1 Ameliorates Glomerular Injury in Progressive Glomerulonephritis

• Material Type: 博士論文
• Title: Conditional Deletion of Smad1 Ameliorates Glomerular Injury in Progressive Glomerulonephritis
• Author/Editor: Araki, Makoto; Matsubara, Takeshi; Abe, Hideharu; Torikoshi, Kazuo; Mima, Akira; Iehara, Noriyuki; Fukatsu, Atsushi; Kita, Toru; Arai, Hidenori; Doi, Toshio
• Author Heading: Araki, Makoto; Matsubara, Takeshi; Abe, Hideharu; Torikoshi, Kazuo; Mima, Akira; Iehara, Noriyuki; Fukatsu, Atsushi; Kita, Toru; Arai, Hidenori; Doi, Toshio
• Publication, Distribution, etc.: Springer nature
• Publication Date: 2016-08-05
• Publication Date (W3CDTF): 2016-08-05
• Alternative Title: Smad1の条件付き遺伝子削除は進行性糸球体腎炎による糸球体傷害を改善する
• Periodical title: Scientific Reports
• No. or year of volume/issue: 6
• Volume: 6
• Pages: 31216-
• ISSN (Periodical Title): ISSN : 2045-2322
• Degree grantor/type: 徳島大学
• Date Granted: 2017-11-30
• Dissertation Number: 乙第2098号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: Glomerulonephritis; Glomerulosclerosis; Collagen type IV; Smad1
• Target Audience: 一般
• Note (General): Matrix expansion and cell proliferation are concomitantly observed in various glomerular injuries. However, the molecular mechanisms responsible for these changes have not been fully elucidated. We have reported that Smad1 is a key signalling molecule that regulates the transcription of type IV collagen (Col4) in mesangial matrix expansion and is thereby involved in glomerular injury in an acute model of glomerulonephritis. In this study, we addressed the role of Smad1 signalling in accelerated nephrotoxic nephritis (NTN), a model of progressive glomerulonephritis, using conditional deletion of Smad1 in Rosa26CreERT2 mice (Smad1-CKO). Mesangial matrix expansion in the Smad1-CKO mice with NTN was significantly inhibited compared with that in wild type mice with NTN, which was consistent with the decrease in Col4 expression level. On the other hand, STAT3 activation and cell proliferation were not influenced by Smad1 deletion in the NTN model. Therefore, we investigated another factor that activates cell proliferation in the absence of Smad1. Id2 induced VEGF secretion and subsequent STAT3 activation, independently of Smad1 expression in mouse mesangial cells. Here we show that Smad1 plays an important role in the development of glomerular injury without affecting cell proliferation, in progressive glomerulonephritis.
• Format (IMT): application/pdf
• Access Restrictions: インターネット公開
• Rights (production): © The Author(s) 2016. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
• Related Material (DOI): 10.1038/srep31216
• 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): 徳島大学 : 徳島大学機関リポジトリ

Table of Contents

https://repo.lib.tokushima-u.ac.jp/files/public/11/110997/2018010915362972490/o2098_abstract_review.pdf fulltext

https://repo.lib.tokushima-u.ac.jp/files/public/11/110997/2018011015375094881/o2098_fulltext.pdf fulltext