Figure 1.Schematic diagram of modes of endothelial cell-vascular smooth muscle cell interaction that may lead to atherosclerosis. Vascular smooth muscle cell phenotypic modulation in culture is associated with reorganisation of contractile and cytoskeletal proteins. Emerging evidence demonstrates that both direct and indirect interplay between ECs and VSMCs are functional. The Phenotypic Switch of Vascular Smooth Muscle Cells: A Key Event in Atherosclerosis and Restenosis. Cell Motil Cytoskeleton. Vascular smooth muscle cells (VSMCs) are a major cell type present at all stages of an atherosclerotic plaque. The role of smooth muscle cells in atherosclerosis. 2004; 94:863–865. In atherosclerosis, the vascular smooth muscle cell (VSMC) contributes to vessel wall inflammation and lipoprotein retention, as well as to the formation … 1997; 135:19–27. Feil S, Hofmann F, Feil R. SM22alpha modulates vascular smooth muscle cell phenotype during atherogenesis. Vascular smooth muscle cells (VSMCs) exhibit phenotypic and functional plasticity in order to respond to vascular injury. Key Words: atherosclerosis extracellular matrix interleukin platelet-derived growth factor smooth muscle Vascular Smooth Muscle Cells in Atherosclerosis Martin R. Bennett, Sanjay Sinha, Gary K. Owens Circulation Research Compendium on Atherosclerosis Atherosclerosis: Successes, Surprises, and Future Challenges 1 The majority of VSMCs in the plaque are derived from the medial layer of the blood vessel. Vascular smooth muscle cells (VSMCs) constitute the major cells in the media layer of arteries, and are critical to maintain the integrity of the arterial wall. Curr Opin Lipidol. In case of the vessel damage, VSMCs are able to switch from the quiescent ‘contractile’ phenotype to the ‘proinflammatory’ phenotype. Vascular smooth muscle cells (VSMCs) constitute the major cells in the media layer of arteries, and are critical to maintain the integrity of the arterial wall. Crossref Medline Google Scholar; 22 Worth NF, Rolfe BE, Song J, Campbell GR. Crossref Medline Google Scholar; 12. Circ Res. Atherosclerosis. Vascular smooth muscle cells (VSMCs) exhibit phenotypic and functional plasticity in order to respond to vascular injury. Vascular smooth muscle cells (VSMCs) play a pivotal role in atherogenesis. However, VSMCs in the media are surrounded by a basement membrane, which provides a brake on VSMC proliferation and migration. Apoptosis (programmed cell death) of vascular smooth muscle cells and macrophages has recently been demonstrated in the following: (a) human atherosclerotic plaques; (b) physiological remodelling of the vessel; and (c) a variety of disease states. 1994; 5: 323–330. They participate in arterial wall remodeling, and play important roles in atherosclerosis throughout all stages of the disease. Subendothelial smooth muscle cells of human aorta express macrophage antigen in situ and in vitro. In case of the vessel damage, VSMCs are able to switch from the quiescent ‘contractile’ phenotype to the ‘proinflammatory’ phenotype. KEYWORDS: Atherosclerosis, Hutchinson-Gilford progeria syndrome, lamin A, progerin, vascular smooth muscle cells Characteristics of Hutchinson-Gilford progeria syndrome (HGPS) HGPS is a premature aging disease that was first described by Jonathan Hutchinson in 1886 and Hastings Gilford in 1897 [ 1 , 2 ]. Link Google Scholar; 13. VSMC can modulate their phenotype) in response to the environmental stimuli via a process characterized by decreased gene expression of VSMC contractile markers and increased proliferation, migration, and matrix synthesis . 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