[Involvement of platelet collagen receptors in primary hemostasis]

At sites of vassel injury, platelets adhere to various components of the subendothelial matrices (SEM). Platelets can interact with several SEM proteins, but of principal importance are collagens and von Willebrand Factor (vWF). The initial entrapment of platelets on subendothelial collagenes requires vWF which under high shear rates conditions created by rapid blood flow present in arteries binds simultaneously to collagen and the platelet glycoprotein complex GPIb/IX/V. Adhered platelets are activated by intracellular signaling pathways and resultant activation of integrin alpha(IIb)beta3 on platelet membranes leads to platelet aggregation by its interaction with vWF or with fibrinogen. The role of GPIb/IX/V for intracellular signaling and integrin alpha(IIb)beta3 activation has remained controversial for a long time. It was assumed that the GPIb/ IX/V/vWF interaction only provides a physical force which fixes platelets to SEM, but now it is evident that the GPIb/IX/V complex mediates signaling which leads to platelet activation. This review will address the molecular mechanisms of platelet function with emphasis on the role of vWF and GPIb/IX/V complex in mediating platelet interaction with the vessel wall.