Abstract
Phenotypic modulation of vascular smooth muscle cells (SMCs) plays an integral role in both vascular development and vasculoproliferative disorders. SMC-specific marker genes include caldesmon, smooth muscle myosin heavy chain, α-smooth muscle actin, calponin, SM22α, and α- and β-tropomyosins. Studies aimed at understanding the role of coactivators and corepressors of phenotypic modulation of SMC have been stimulated by the cloning and characterization of these SMC-specific genes and the discovery that the widely expressed serum response factor (SRF) is central to the expression of SMC-specific genes. SRF directly regulates the coordinated expression of several contractile and cytoskeletal genes through one or more CArG-box elements in the regulatory sequences of SMC-specific genes. This CArG-dependent program of SMC differentiation is modulated during both vascular development and arterial remodeling.1 Myocardin and myocardin-related transcription factors (MRTFs) bind to SRF, potently stimulate SRF-dependent transcription, and are necessary and sufficient for SMC differentiation.2 The RhoA pathway appears to activate myocardins by …
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