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タイトル: Conditional Deletion of Smad1 Ameliorates Glomerular Injury in Progressive Glomerulonephritis
著者: Araki, Makoto
Matsubara, Takeshi
Abe, Hideharu
Torikoshi, Kazuo
Mima, Akira
Iehara, Noriyuki
Fukatsu, Atsushi
Kita, Toru
Arai, Hidenori
Doi, Toshio
著者名の別形: 荒木, 真
松原, 雄
鳥越 , 和雄
家原, 典之
深津, 敦司
キーワード: Nephritis
Transcription
発行日: 5-Aug-2016
出版者: Springer Nature
誌名: Scientific Reports
巻: 6
論文番号: 31216
抄録: 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.
著作権等: © 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.
URI: http://hdl.handle.net/2433/227129
DOI(出版社版): 10.1038/srep31216
出現コレクション:学術雑誌掲載論文等

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