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Myocardin‐related transcription factor‐A induces cardiomyocyte hypertrophy
Author(s) -
Liao XingHua,
Wang Nan,
Liu QingXi,
Qin Tao,
Cao Bo,
Cao DongSun,
Zhang TongCun
Publication year - 2011
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.415
Subject(s) - myocardin , serum response factor , muscle hypertrophy , calponin , myocyte , biology , transcription factor , endocrinology , medicine , phenylephrine , microbiology and biotechnology , coactivator , downregulation and upregulation , gene , smooth muscle , genetics , blood pressure
Myocardin is a remarkably potent transcriptional coactivator expressed specifically in cardiac muscle lineages and smooth muscle cells during postnatal development. Myocardin shares homology with myocardin‐related transcription factor‐A (MRTF‐A), which are expressed in a broad range of embryonic and adult tissues. Our previous results show that myocardin induces cardiac hypertrophy. However, the effects of MRTF‐A in cardiac hypertrophy remain poorly understood. Our present work further demonstrates that myocardin plays an important role in inducing hypertrophy. At the same time, we find that overexpression of MRTF‐A in neonatal rat cardiomyocytes might induce cardiomyocyte hypertrophy. Furthermore, MRTF‐A expression is induced in phenylephrine, angiotensin‐II, and transforming growth factor‐β‐stimulated cardiac hypertrophy, whereas a dominant‐negative form of MRTF‐A or MRTF‐A siRNA strongly inhibited upregulation of hypertrophy genes in response to hypertrophic agonists in neonatal rat cardiomyocytes. Our studies indicate that besides myocardin, MRTF‐A might play an important role in cardiac hypertrophy. Our findings provide novel evidence for the future studies to explore the roles of MRTFs in cardiac hypertrophy. © 2011 IUBMB IUBMB Life, 63(1):54–61, 2011.