Platelets, platelet-derived growth factor and arteriosclerosis

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Abstract
Platelets participate in the pathogenesis of arteriosclerosis and in the progression of atherosclerosis by adhering to the damaged arteries and subsequently forming mural thrombi which are either swept away and embolize or are endothelialized and thus become part of the vessel wall. Rheologic considerations predict and blood perfusion experiemnts using flow chambers with exposed vessel wall components demonstrate that platelet participation increases with the wall shear rate and is thus particularly important in stenosed arteries (acute thrombosis) and the microvasculature (hemostasis). In addition to their involvement in thrombosis, activated platelets release growth factors, most notably a platelet-derived growth factor (PDGF) which may be the principal mediator of smooth muscle cell migration from the media into the intima and of smooth muscle cell proliferation in the intima as well as of vasoconstriction. The recent discovery that PDGF can be produced by additional cells involved in the pathogenesis of arteriosclerosis (endothelial cells, monocytes/macrophages, smooth muscle cells themselves) and that they may play a role in tumorigenesis has tremendously increased the interest in this growth factor and in potential antagonists.