Abstract

Vascular smooth muscle cell (VSMC) differentiation is determined primarily by the level and activity of serum response factor and myocardin, which constitute a potent transcriptional switch over CArG elements located near a growing number of VSMC protein coding and non-coding RNA genes. Unlike the other two muscle types, differentiated VSMC are intrinsically wired to display a range of phenotypes that include embryonic forms of VSMC and disparate cell types that arise through a transdifferentiation-like process. This phenotypic adaptation occurs in response to aberrant signaling inputs and changes in VSMC gene expression associated with pathological insults to the vessel wall. In this chapter, several examples of VSMC phenotypic adaptation will be presented to highlight the critical role of serum response factor and myocardin in maintaining normal VSMC homeostasis.

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