Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 28, Issue 8, Pages 1505-1510Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.108.166066
Keywords
smooth muscle; serum response factor; myocardin; contraction; knockdown
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Funding
- NHLBI NIH HHS [HL077726, HL62572, R01 HL091168, R01 HL132574, R01 HL062572-11, R01 HL077726, R01 HL062572] Funding Source: Medline
- NIA NIH HHS [R42 AG026950, R37 AG023084, AG026950, R41 AG026950, AG023084, R01 AG023084] Funding Source: Medline
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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. Conclusion - Myocd is sufficient for the establishment of a SMC-like contractile phenotype.
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