Document Detail

miR-101 Inhibited Post-Infarct Cardiac Fibrosis and Improved Left Ventricular Compliance via FOS/TGFβ1 Pathway.
MedLine Citation:
PMID:  22811578     Owner:  NLM     Status:  Publisher    
BACKGROUND: Cardiac interstitial fibrosis is a major cause of the deteriorated performance of the heart in patients with chronic myocardial infarction. MicroRNAs have recently been proven a novel class of regulators of cardiovascular diseases, including those associated with cardiac fibrosis. This study aimed to explore the role of miR-101 in cardiac fibrosis and the underlying mechanisms. METHODS AND RESULTS: Four weeks after coronary artery ligation of rats, the expression of miR-101a and miR-101b (miR-101a/b) in the peri-infarct area was decreased. Treatment of cultured rat neonatal cardiac fibroblasts (CFs) with angiotensin II (AngII) also suppressed the expression of miR-101a/b. Forced expression of miR-101a/b suppressed the proliferation and collagen production in rat neonatal CFs, as revealed by cell counting, MTT assay and qRT-PCR. The effect was abrogated by co-transfection with AMO-101a/b, the antisense inhibitors of miR-101a/b. c-Fos was found to be a target of miR-101a as overexpression of miR-101a decreased the protein and mRNA levels of c-Fos and its downstream protein TGFβ1. Silencing c-Fos by small interfering RNA mimicked the anti-fibrotic action of miR-101a, whereas forced expression of c-Fos protein canceled the effect of miR-101a in cultured CFs. Strikingly, echocardiography and hemodynamic measurements indicated remarkable improvement of the cardiac performance 4-weeks after adenovirus mediated overexpression of miR-101a in rats with chronic myocardial infarction. Furthermore, the interstitial fibrosis was alleviated and the expression of c-Fos and TGFβ1 was inhibited. CONCLUSIONS: Overexpression of miR-101a can mitigate interstitial fibrosis and the deterioration of cardiac performance in post-infarct rats, indicating the therapeutic potential of miR-101a for cardiac disease associated with fibrosis.
Zhenwei Pan; Xuelin Sun; Hongli Shan; Ning Wang; Jinghao Wang; Jinshuai Ren; Shuya Feng; Liangjun Xie; Chunying Lu; Ye Yuan; Yang Zhang; Ying Wang; Yanjie Lu; Baofeng Yang
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-7-18
Journal Detail:
Title:  Circulation     Volume:  -     ISSN:  1524-4539     ISO Abbreviation:  -     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-7-19     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Harbin Medical University, Harbin, China.
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