Review |
From the Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville.
Correspondence to Gary K. Owens, PhD, Department of Molecular Physiology and Biological Physics, University of Virginia, MR5 Rm 1220, 415 Lane Rd, PO box 801394, Charlottesville, VA 22908. E-mail gko{at}virginia.edu
This Review is part of a thematic series on Vascular Cell Diversity, which includes the following articles:
Heart Valve Development: Endothelial Cell Signaling and Differentiation
Molecular Determinants of Vascular Smooth Muscle Cell Diversity
Endothelial/Pericyte Interaction
Endothelial-ECM: Biosynthesis, Remodeling, and Functions
Joyce Bischoff Guest Editor
Although the primary role of vascular smooth muscle cells (SMCs) is contraction, they exhibit extensive phenotypic diversity and plasticity during normal development, during repair of vascular injury, and in disease states. Results of recent studies indicate that there are unique as well as common transcriptional regulatory mechanisms that control expression of various SMC marker genes in distinct SMC subtypes, and that these mechanisms are complex and dynamic even at the single cell level. This article will review recent progress in our understanding of the transcriptional regulatory mechanisms involved in controlling expression of SMC marker genes with a particular focus on examination of processes that contribute to the phenotypic diversity of SMCs. In addition, because of considerable controversy in the literature regarding the relationship between phenotypically modulated SMCs and myofibroblasts, we will briefly consider both similarities and differences in regulation of gene expression between these cell types.
Key Words: smooth muscle cells serum response factor myofibroblasts
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