The smooth muscle cell is another major component — and progenitor — of the fatty streak [Hajjar DP and Nicholson AC, 1995]. Along with macrophages, smooth-muscle cells (which normally lie in the medial layer and are responsible for maintaining vascular tone) proliferate in the intima during atherogenesis.
Proliferation of smooth muscle cells within the intima makes up a substantial bulk of the atherosclerotic lesion, which may rise several millimeters above the surface of the surrounding intima. A number of molecular factors may play a role in the proliferation and migration of smooth-muscle cells. They include growth factors (eg, platelet-derived growth factor, or PDGF, a polypeptide released from blood platelets and endothelial cells that may attract smooth-muscle cells to the intima and encourage them to divide), eicosanoids (which can stimulate the hydrolysis of cholesteryl ester, producing free cholesterol), certain cytokines (eg, tumor necrosis factor, interleukin-1 and interferon), and nitric oxide (which acts to dilate blood vessels) [Hajjar DP and Nicholson AC, 1995].
Acute Ischemic Stroke: New Concepts of Care
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