Myocardin is sufficient for a smooth muscle-like contractile phenotype

Xiaochun Long, Robert D. Bell, William T. Gerthoffer, Berislav V. Zlokovic, Joseph M. Miano

Research output: Contribution to journalArticlepeer-review

86 Scopus citations

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 BC3H1 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 BC3H1 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. Conclusion - Myocd is sufficient for the establishment of a SMC-like contractile phenotype.

Original languageEnglish (US)
Pages (from-to)1505-1510
Number of pages6
JournalArteriosclerosis, thrombosis, and vascular biology
Volume28
Issue number8
DOIs
StatePublished - Aug 2008

Keywords

  • Contraction
  • Knockdown
  • Myocardin
  • Serum response factor
  • Smooth muscle

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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