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Thrombus determinants of vascular cell activation.

Vascular wall remodeling after arterial injury involves the migration and proliferation of smooth muscle cells (SMCs) into the intima and the development of a neointima that reduces luminal diameter. Many factors may play a role in SMC proliferation, including platelet-derived mitogens and thrombin1,2. The cellular events associated with neointimal proliferation in response to vascular injury may be induced in part by the platelet-rich thrombus that forms at the site of vascular injury. Platelet-rich thrombosis is dependent on a dynamic interaction between platelet adhesion and aggregation, exposure of membrane-bound tissue factor (TF), elaboration of factor Xa by the TF/VII complex, and localization of the Xa/Va complex on a phospholipid surface most likely provided by adherent platelets (Fig. 1). Platelet adhesion is mediated by specific binding of platelet membrane receptors to the subendothelial adhesive glycoproteins such as collagen, and subsequent platelet deposition is determined by several mechanisms, including extent of arterial injury, shear-dependent platelet adhesion and aggregation and elaboration of platelet agonists.