© 1996 American Heart Association, Inc.
Articles |
Role of Mechanical Strain in Regulation of Differentiation of Vascular Smooth Muscle Cells
Correspondence to Dr Gary K. Owens, Department of Molecular Physiology and Biological Physics, P.O. Box 10011, University of Virginia School of Medicine, Charlottesville, VA 22906-0011.
Key Words: mechanical strain • vascular smooth muscle cells
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Introduction |
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The differentiated vascular smooth muscle cell (SMC) is a highly specialized cell that expresses a unique repertoire of contractile proteins, ion channels, membrane receptors, and signaling molecules necessary for its contractile function (reviewed in Reference 1). The SMC, however, is not terminally differentiated and is capable of undergoing marked changes in phenotype in response to changes in local environmental cues that normally control its differentiation/maturation. For example, after vessel injury, fully differentiated medial SMCs undergo a process referred to as "phenotypic modulation," which is characterized by decreased expression of markers of differentiated SMCs, such as smooth muscle
-actin and smooth muscle myosin heavy chain (SM MHC), and by accelerated growth and increased synthesis of extracellular matrix components, which are important for repair of the damaged vessel.1 2 SMCs within atherosclerotic lesions also exhibit marked differences in morphology and protein expression patterns compared with normal medial SMCs.3 4 Importantly, phenotypic changes in intimal SMCs are clearly not simply a function of the growth state of the SMC, since alterations persist even when growth rates return to normal.5 Of particular significance, phenotypic alterations in intimal SMCs within atherosclerotic lesions include not only enhanced growth responsiveness but also altered lipid metabolism and increased matrix production, which are likely to play a major role in the development and/or progression of atherosclerosis. Despite the importance of changes in SMC phenotype in atherogenesis, surprisingly little is known regarding the mechanisms and factors that normally control the differentiation of the SMC and how these control processes are altered in This article has been cited by other articles:
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