期刊
CELLULAR SIGNALLING
卷 27, 期 12, 页码 2410-2424出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2015.09.005
关键词
Hsp90; Cdc37; Angiotensin-II; TGF beta receptor-II; Cardiac hypertrophy; Collagen
类别
资金
- Department of Biotechnology
- Council of Scientific and Industrial Research (CSIR), India [09/028(0834)/2011-EMR-I]
- Department of Science and Technology, Govt. of India
Cardiac hypertrophy is accompanied by excessive collagen deposition in the heart. Despite painstaking research on this fatal disease, the precise role of molecular chaperones in myocardial fibrosis has not yet been elucidated. In this study, we have analyzed the mechanism by which Heat shock protein 90 (Hsp90)/Cell division cycle 37 (Cdc37) assembly modulates cardiac hypertrophy associated fibrosis. For the in vitro hypertrophy model, Angiotensin II (AngII) treated cultured adult cardiac fibroblasts were used, whereas the in vivo hypertrophy model was generated by renal artery ligation in adult male Wistar rats (Rattus norvegicus). Pretreatment with the Hsp90 inhibitor or the blocking of Hsp90-Cdc37 interactions during pressure overload hypertrophy resulted in ubiquitin-mediated proteasomal degradation of TGF beta receptor-II (T beta R-II) leading to termination of TGF beta mediated signaling. In both cases significant reduction in collagen synthesis was observed revealing the Hsp90/Cdc37 complex as an integral profibrotic component of TOM, signaling during cardiac hypertrophy. (C) 2015 The Authors. Published by Elsevier Inc.
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