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Arterioscler Thromb Vasc Biol. 2008 Aug;28(8):1505-10. doi: 10.1161/ATVBAHA.108.166066. Epub 2008 May 1.

Myocardin is sufficient for a smooth muscle-like contractile phenotype.

Author information

1
Aab Cardiovascular Research Institute, University of Rochester School of Medicine & Dentistry, 211 Bailey Road, Rochester, New York 14586, USA.

Abstract

BACKGROUND:

Myocardin (Myocd) is a strong coactivator that binds the serum response factor (SRF) transcription factor over CArG elements embedded within smooth muscle cell (SMC) and cardiac muscle cyto-contractile genes. Here, we sought to ascertain whether Myocd-mediated gene expression confers a structural and physiological cardiac or SMC phenotype.

METHODS AND RESULTS:

Adenoviral-mediated expression of Myocd in the BC(3)H1 cell line induces cardiac and SMC genes while suppressing both skeletal muscle markers and cell growth. Immunofluorescence microscopy shows that SRF and a SMC-like cyto-contractile apparatus are elevated with Myocd overexpression. A short hairpin RNA to Srf impairs BC(3)H1 cyto-architecture; however, cotransduction with Myocd results in complete restoration of the cyto-architecture. Electron microscopic studies demonstrate a SMC ultrastructural phenotype with no evidence for cardiac sarcomerogenesis. Biochemical and time-lapsed videomicroscopy assays reveal clear evidence for Myocd-induced SMC-like contraction.

CONCLUSIONS:

Myocd is sufficient for the establishment of a SMC-like contractile phenotype.

PMID:
18451334
PMCID:
PMC2574857
DOI:
10.1161/ATVBAHA.108.166066
[Indexed for MEDLINE]
Free PMC Article
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