Myosin isoform expression and smooth muscle cell heterogeneity in normal and atherosclerotic rabbit aorta.

Abstract

234 SMC that accumulate in arterial intima show morphological features that are distinct from those in the medial SMC, including myofilaments, rough endoplasmic reticulum, free ribosomes, and mitochondria. 456 A differential distribution of synthetic organelles and myofilaments can also be demonstrated in cultured vascular SMC 7 and the intimal thickening that follows endothelial injury. 6 The structural and synthetic profile of developing smooth muscle (SM) tissue has some features in common with proliferating SMC found in the first stages of intimal thickening. 8 In this system, after cessation of cell division, SMC partly resume the adult differentiated morphology.9 According to some authors, SMC showing differentiated characteristics are unable to proliferate, and the term "phenotypic modulation" has been used 510 to indicate the existence

Nifedipine Inhibits Vascular Smooth Muscle Cell Dedifferentiation via Downregulation of Akt Signaling

“…[2][3][4] These changes are accompanied by alterations in the expression of phenotypic markers, such as smooth muscle ␣-actin, smooth muscle myosin heavy chain (SM2), and nonmuscle myosin heavy chain (SMemb). 1,5 The phosphatidylinositol 3-kinase/Akt signaling pathway is involved in regulating the phenotypic changes of VSMCs. The Akt signaling is activated by certain growth factors, such as platelet-derived growth factor (PDGF), which influences the phenotype of VSMCs.…”

Aortic intimal thickening and myosin isoform expression in hyperthyroid rabbits.

“…Intimal SMCs show the same myosin isoform pattern, that is, coexpression of SM and NM myosin of the developing aorta and cultured aortic SMCs. 8 Similar to hyperthyroidism, hypercholesterolemia is characterized by a migration/ proliferation of medial SMCs into the intima. 2324 The predominant SMC population of the plaque and the majority of medial SMCs present in the underlying media share the same myosin isoform pattern reported here for hyperthyroid rabbits.…”

“…In the aortic media from thyroxinetreated rabbits, the number of medial SMCs reactive for desmin ( Figure 2B) and NM myosin ( Figure 2D) was markedly increased compared with the normal euthyroid rabbits ( Figures 2E and 2F), whereas no visible change could be seen with anti-vimentin (Figure 2A) or anti-SM myosin ( Figure 2C) antibodies. In the aortic wall of normal euthyroid rabbits, antivimentin (L. Giuriato, unpublished observations) and anti-SM myosin 8 antibodies labeled all the medial SMCs, whereas the anti-desmin antibody ( Figure 2E) and anti-NM myosin antibodies stained only a few medial SMCs 8 ( Figure 2F). …”

“…4 -7 -9 In addition, the expression of these two proteins appears to be devel-opmentally regulated in several species. 3 -46 - 17 We have recently demonstrated 8 that the normal aortic media of rabbits contains two smooth muscle cell (SMC) populations, one of which displays a myosin isoform content similar to that found in developing aortic tissue. 6 -8 Two SMC populations with different capacities for growth in the absence of plateletderived growth factor (PDGF) have also been described in cultured SMCs derived from the aortic wall of the adult rat.…”

“…15 The SMC subpopulation with an "immature" type of myosin isoform expression becomes particularly evident in the proliferative events that accompany the development of the atherosclerotic lesion. 8 Cultured SMCs derived from the intimal thickening, obtained from the adult rat by the mechanical denudation tech-nique, and the aortic SMC cultures of newborn rats share some similarities in their PDGF-like activity and transcription of the gene for PDGF-B. 12 -1516 Although the role of growth factors in controlling SMC growth is well established, 14 less is known about the potential effect of hormones on vascular SM tissue.…”