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Myocardin is sufficient for a smooth muscle-like contractile phenotype
Ist Teil von
Arteriosclerosis, thrombosis, and vascular biology, 2008-08, Vol.28 (8), p.1505-1510
Ort / Verlag
United States
Erscheinungsjahr
2008
Quelle
MEDLINE
Beschreibungen/Notizen
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.
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.
Myocd is sufficient for the establishment of a SMC-like contractile phenotype.