Key result
MRTF-A overexpression induced cardiomyocyte hypertrophy, whereas MRTF-A siRNA strongly inhibited hypertrophy gene upregulation in response to agonists in neonatal rat cardiomyocytes.
Why the study?
Does MRTF-A induce cardiomyocyte hypertrophy in neonatal rat cardiomyocytes?
Does MRTF-A induce cardiomyocyte hypertrophy in neonatal rat cardiomyocytes?
MRTF-A plays an important role in inducing cardiomyocyte hypertrophy, providing a potential novel target for future studies on cardiac hypertrophy.
MRTF-A may regulate hypertrophy in vitro; hypothesis-generating for therapeutic targeting pending in vivo and clinical validation.
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.
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Liao et al. (2011) studied Cardiac hypertrophy. MRTF-A overexpression and MRTF-A siRNA was evaluated on Cardiomyocyte hypertrophy and upregulation of hypertrophy genes. MRTF-A overexpression induced cardiomyocyte hypertrophy, whereas MRTF-A siRNA strongly inhibited hypertrophy gene upregulation in response to agonists in neonatal rat cardiomyocytes.
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