ABSTRACT
The development of atherosclerotic lesions is thought to result from endothelial dysfunction, involving alterations in adhesion molecule expression and diminished release of prostacyclin (PGI2) and nitric oxide (NO), which normally inhibit smooth muscle contraction and proliferation, platelet aggregation, and monocyte adhesion to the endothelial surface (1,2). Focal accumulation within the arterial intima of excess amounts of cholesterol-rich low-density lipoprotein (LDL) leads to the migration and recruitment of monocytes into these areas. Monocytes then differentiate into macrophages after taking up large amounts of oxidized LDL via their scavenger receptor to become lipid-laden "foam cells" within the subendothelial space, an early characteristic of the atherosclerotic lesion (3-6). Concomitant release of cytokines, such as interleukin-1, tumor necrosis factor-a, and transforming growth factor-^, by activated lesion macrophages and smooth muscle cells exposed to oxidized LDL modulates smooth muscle cell phenotype and proliferation (7).
