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MiR‐221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression
Author(s) -
Wang Changxin,
Wang Shuiyun,
Zhao Peng,
Wang Xiaojian,
Wang Jizheng,
Wang Yilu,
Song Lei,
Zou Yubao,
Hui Rutai
Publication year - 2012
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24075
Subject(s) - gene knockdown , microrna , hypertrophic cardiomyopathy , muscle hypertrophy , transfection , cardiac myocyte , blot , myocyte , medicine , cardiac hypertrophy , heart failure , biology , downregulation and upregulation , microbiology and biotechnology , cardiology , gene , genetics
Cardiac hypertrophy has been known as an independent predictor for cardiovascular morbidity and mortality. Molecular mechanisms underlying the development of heart failure remain elusive. Recently, microRNAs (miRs) have been established as important regulators in cardiac hypertrophy. Here, we reported miR‐221 was up‐regulated in both transverse aortic constricted mice and patients with hypertrophic cardiomyopathy (HCM). Forced expression of miR‐221 by transfection of miR‐221 mimics increased myocyte cell size and induced the re‐expression of fetal genes, which were inhibited by the knockdown of endogenous miR‐221 in cardiomyocytes. The TargetScan algorithm‐based prediction identified that p27, a cardiac hypertrophic suppressor, is the putative target of miR‐221, which was confirmed by luciferase assay and Western blotting. In conclusion, our results demonstrated that miR‐221 regulated cardiomyocyte hypertrophy probably through down‐regulation of p27, suggesting that miR‐221 may be a new intervention target for cardiac hypertrophy. J. Cell. Biochem. 113: 2040–2046, 2012. © 2012 Wiley Periodicals, Inc.