This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Parmacek, M. S. Search for Related Content PubMed PubMed Citation Articles by Parmacek, M. S.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1535.)
© 2004 American Heart Association, Inc.

Editorials

Myocardin—Not Quite MyoD

Michael S. Parmacek

From the Department of Medicine (Molecular Cardiology), University of Pennsylvania, Philadelphia, Pa.

Correspondence to Michael S. Parmacek, MD, Division of Cardiovascular Medicine, Department of Medicine, University of Pennsylvania School of Medicine, 9123 Founders Pavilion, 3400 Spruce St., Philadelphia, PA 19104, E-mail Michael.parmacek@uphs.upenn.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Smooth muscle cells (SMCs) have evolved to subserve a variety of diverse functions in higher vertebrates, including modulation of arterial tone, regulation of airway resistance, and control of gastrointestinal motility. The diverse functional capacities of SMCs are ultimately determined by the expression of genes encoding SMC-restricted contractile and cytoskeletal proteins, intracellular enzymes, cell surface ligands, and receptors. Several features distinguish the SMC lineage from the skeletal (fast and slow) and cardiac muscle cell lineages. In contrast to skeletal and cardiac muscle cells, SMCs fail to undergo terminal differentiation and permanently exit the cell cycle. In addition, SMCs retain the capacity to reversibly modulate their phenotype during postnatal development in response to a variety of extracellular stimuli including vessel wall injury. As such, the molecular programs underlying SMC differentiation must differ fundamentally from those programs governing skeletal and cardiac myocyte differentiation.

See page 1596

Relatively little is currently understood about the molecular mechanisms that regulate SMC lineage specification, differentiation, and modulation of SMC phenotype. This is because, in part, of the complex embryological origins of the SMC lineage, which are derived both from mesodermally-derived lateral mesenchyme as well as ectodermally-derived neural crest. In addition, in contrast to skeletal and cardiac lineages, relatively few definitive markers of the SMC lineage have been identified, and expression of these markers may be undetectable when SMCs modulate their phenotype from contractile to synthetic (for review see Owens¹). SM-myosin heavy chain (SMyHC) is generally considered the "definitive" SMC marker because it is expressed exclusively in . . . [Full Text of this Article]

This article has been cited by other articles:

				M. S. Parmacek Myocardin-Related Transcription Factors: Critical Coactivators Regulating Cardiovascular Development and Adaptation Circ. Res., March 16, 2007; 100(5): 633 - 644. [Abstract] [Full Text] [PDF]