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MicroRNA‐214 exerts a Cardio‐protective effect by inhibition of fibrosis
Author(s) -
Dong Hua,
Dong Shimin,
Zhang Lisi,
Gao Xueping,
Lv Guangwei,
Chen Wei,
Shao Suxia
Publication year - 2016
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.23396
Subject(s) - microrna , fibrosis , pharmacology , medicine , cancer research , biology , genetics , gene
The miRNAs play important roles in regulating myocardial fibrosis. The purpose of this study was to determine the potential roles of microRNA‐214 (miR‐214) in cardiac fibrosis in vitro and in vivo . In vitro experiment, Ang II‐induced cardiac fibroblasts (CFBs) are transfected with pre‐miR‐214, anti‐miR‐214 and their oligo controls. Gene expression was checked by Quantitative realtime‐PCR (qRT‐PCR) and western blotting. In the present experiment, compared with controls, expressions of collagen type I (COL I), collagen type III (COL III), transforming growth factor (TGF)‐β1, and tissue inhibitors of metalloproteinase (TIMP)‐1 were all increased, but matrix metalloproteinase (MMP)‐1 was reduced in CFB by Ang II treatment at both mRNA and protein levels, and these alterations were found reversed by miR‐214 transfection. In vivo , an anterior transmural acute myocardial infarction (AMI) was created by occlusion of the left anterior descending coronary artery after Ad‐pre‐miR‐214, Ad‐anti‐miR‐214 or Ad‐GFP was delivered separately. Four weeks after AMI, protein contents of COL I, COL III and TGF‐β1 in tissue from border area were found increased after AMI, but impaired by overexpression of miR‐214. While the expression of MMP‐1 was increased by miR‐214 stimulation but decreased by miR‐214 inhibition. These results suggested that miR‐214 exerts cardio‐protective effects by inhibition of fibrosis and the inhibitory effect involves TGF‐β1 suppression and MMP‐1/TIMP‐1 regulation. Anat Rec, 299:1348–1357, 2016. © 2016 Wiley Periodicals, Inc.