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Circulation Research. 2006;98:1089-1097
Published online before print March 23, 2006, doi: 10.1161/01.RES.0000218781.23144.3e
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(Circulation Research. 2006;98:1089.)
© 2006 American Heart Association, Inc.

Integrative Physiology

Myocardin Induces Cardiomyocyte Hypertrophy

Weibing Xing*, Tong-Cun Zhang*, Dongsun Cao, Zhigao Wang, Christopher L. Antos, Shijie Li, Yibin Wang, Eric N. Olson, Da-Zhi Wang

From the Carolina Cardiovascular Biology Center (W.X., T.-C.Z., D.C., D.-Z.W.), Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill; the Department of Molecular Biology (Z.W., C.L.A., S.L., E.N.O.), University of Texas Southwestern Medical Center, Dallas; and the Division of Molecular Medicine (Y.W.), David Geffen School of Medicine, UCLA, Los Angeles, California.

Correspondence to Da-Zhi Wang, Carolina Cardiovascular Biology Center, Department of Cell and Developmental Biology, 103 Mason Farm Rd, University of North Carolina, Chapel Hill, NC 27599-7126. E-mail dawang{at}med.unc.edu

In response to stress signals, postnatal cardiomyocytes undergo hypertrophic growth accompanied by activation of a fetal gene program, assembly of sarcomeres, and cellular enlargement. We show that hypertrophic signals stimulate the expression and transcriptional activity of myocardin, a cardiac and smooth muscle–specific coactivator of serum response factor (SRF). Consistent with a role for myocardin as a transducer of hypertrophic signals, forced expression of myocardin in cardiomyocytes is sufficient to substitute for hypertrophic signals and induce cardiomyocyte hypertrophy and the fetal cardiac gene program. Conversely, a dominant-negative mutant form of myocardin, which retains the ability to associate with SRF but is defective in transcriptional activation, blocks cardiomyocyte hypertrophy induced by hypertrophic agonists such as phenylephrine and leukemia inhibitory factor. Myocardin-dependent hypertrophy can also be partially repressed by histone deacetylase 5, a transcriptional repressor of myocardin. These findings identify myocardin as a nuclear effector of hypertrophic signaling pathways that couples stress signals to a transcriptional program for postnatal cardiac growth and remodeling.


Key Words: cardiac hypertrophy • cardiac myocytes • cardiac transcription factors • myocardin • serum response factor • transcription factors • transcriptional regulation


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