Redundancy and Interaction of Thrombin- and Collagen-Mediated Platelet Activation in Tail Bleeding and Carotid Thrombosis in Mice

Abstract

The observation that loss of Par4 uncovered large effects of GPVI deficiency implies that Par4 and GPVI made independent, partially redundant contributions to occlusive thrombus formation in the carotid and to hemostatic clot formation in the tail under the experimental conditions examined. At face value, these results suggest that thrombin- and collagen-induced platelet activation can play partially redundant roles, despite important differences in how these agonists are made available to platelets.