Platelets and Atherogenesis in Normal and von Willebrand Disease Pigs

Abstract

There is increasing evidence that platelet-arterial wall interaction is an important step in the genesis of arteriosclerotic lesions (1). The genesis of these lesions may involve the following factors (2): (a) continued endothelial injury; (b) adherence and aggregation of platelets to damaged endothelial cells or to exposed subendothelial tissue; (c) local release of platelet constituents, including a mitogenic protein (platelet-derived growth factor) that stimulates growth of cultured smooth muscle cells, and passage of such platelet constituents into the underlying arterial wall; (d) migration of smooth muscle cells through the internal elastic lamina into the intima and platelet-mediated intimal proliferation of smooth muscle cells; (e) formation of a connective tissue matrix by the smooth muscle cells through synthesis and secretion of collagen, elastic fiber proteins, and glycosaminoglycans; and (f) accumulation of intracellular and extracellular lipids.