Examination of the earliest cellular events that occur during atherogenesis has demonstrated a specialized type of chronic inflammatory response that precedes migration and proliferation of arterial smooth muscle cells. The first observable events include increased accumulation of lipid and lipoprotein particles beneath the endothelium, presumably from increased transport and/or permeability of the lining endothelial cells. This event is rapidly followed by attachment, adherence, and spreading of peripheral blood monocytes and T-lymphocytes at sites throughout the arterial tree, particularly at branches and bifurcations. These cells adhere from the formation of adhesive cell-surface glycoproteins by the endothelium and the leukocytes, which interact in a ligand-receptor manner. Thus one of the earliest changes induced by hypercholesterolemia and hypertension appears to be altered endothelial permeability, together with the adherence of leukocytes, representing the first phase of an inflammatory response. The leukocytes migrate across the surface of the endothelium, probe between the junctions of the endothelial cells, and are chemotactically attracted into the subendothelial space where they begin to accumulate within the intima. In the presence of oxidized low-density lipoprotein, the monocytes become converted to activated macrophages and, through their scavenger receptors, take up the modified lipoprotein particles and become foam cells. The
American Heart Journal – Elsevier
Published: Nov 1, 1999
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