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1 Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, Virginia, United States; Department of Medicine and Biological Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
2 Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, Virginia, United States
* To whom correspondence should be addressed. E-mail: gko{at}virginia.edu.
Smooth muscle cell (SMC) differentiation is an essential component of vascular development and these cells perform biosynthetic, proliferative and contractile roles in the vessel wall. SMC are not terminally differentiated and possess the ability to modulate their phenotype in response to changing local environmental cues. The focus of this review is to provide an overview of the current state of knowledge of molecular mechanisms involved in controlling phenotypic switching of SMC with particular focus on examination of processes that contribute to the repression of SMC marker genes. We discuss environmental cues which actively regulate SMC phenotypic switching such as PDGF-BB as well as several important regulatory mechanisms required for suppressing expression of SMC specific/selective marker genes in vivo, including those dependent on conserved G/C-repressive elements, and/or highly conserved degenerate CArG elements found in the promoters of many of these marker genes. Finally, we present evidence indicating that SMC phenotypic switching involves multiple active repressor pathways including KLF4, HERP, and ERK-dependent phosphorylation of Elk-1 that act in a complimentary fashion.
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