Vascular injury: platelets and smooth muscle cell response

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Abstract
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 [ 3 H]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 form the basis for a modification of the hypothesis implicating platelets in atherogenesis.

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