Abstract
Smooth muscle cells play a major role in the formation of the vascular lesions found in atherosclerosis and restenosis injury after angioplasty [1,2]. The smooth muscle cells found in such lesions show reduced levels of many markers of the differentiated state of smooth muscle (e.g. SM22α, smooth muscle-myosin heavy chain {SM-MHC} and smooth muscle α-actin {Smα-actin} [3,4]). In some instances the smooth muscle-specific isoforms of contractile proteins (e.g. SM-MHC) are replaced by their non-muscle equivalents. In addition to loss of expression of smooth muscle-specific genes, intimal vascular smooth muscle cells (VSMCs) express genes that are associated with calcium metabolism in bone tissue (e.g. matrix GLA protein and osteopontin [5–8]). There has been significant progress towards identifying the factors involved in promoting or inhibiting smooth muscle cell proliferation in these pathologic conditions. However, little is known about the mechanisms that regulate the differentiated state of this cell type or the factors involved in defining smooth muscle phenotype [9]. Given the phenotypic changes seen in VSMC in pathological conditions, the systems which control the differentiated state of smooth muscle may play a significant role in lesion formation.
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Kemp, P.R., Metcalfe, J.C. (1999). Expression of Basic Helix-Loop-Helix Proteins and Smooth Muscle Phenotype in the Adult Rat Aorta. In: Doevendans, P.A., Reneman, R.S., van Bilsen, M. (eds) Cardiovascular Specific Gene Expression. Developments in Cardiovascular Medicine, vol 214. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9321-2_20
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DOI: https://doi.org/10.1007/978-94-015-9321-2_20
Publisher Name: Springer, Dordrecht
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