Vascular injury: platelets and smooth muscle cell response.
The blood platelet appears to play an important role in the pathogenesis of the atherosclerotic plaque. Using a platelet specific antigen, platelet factor 4 (PF4), we have demonstrated that PF4 released from platelets enters the vessel wall. Smooth muscle cell (s.m.c.) proliferation in vivo was examined by using a new technique for measuring [3H]thymidine incorporation. With this technique, we have shown that a remote vascular injury can cause s.m.c. proliferation, presumably mediated by a humoral agent. Endothelial dysfunction, in turn, may be caused by a sustained, mild hypercholesterolaemia. This permeability dysfunction may provide circulating s.m.c. mitogens with access to the vessel, wall, thus allowing s.m.c. proliferation in areas of non-desquamated endothelium. These experiments from the basis for a modification of the hypothesis implicating platelets in atherogenesis.
D000818:Animals; D001011:Aorta / Q000293:injuries*; D001161:Arteriosclerosis / Q000209:etiology*; D001779:Blood Coagulation Factors / Q000378:metabolism*; D002455:Cell Division / Q000187:drug effects; D004195:Disease Models, Animal; D004727:Endothelium / Q000166:cytology; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D010978:Platelet Factor 4 / Q000378:metabolism* / Q000494:pharmacology; D011817:Rabbits
D001779:Blood Coagulation Factors; D010978:Platelet Factor 4