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Thrombus formation is initiated when circulating von Willebrand factor (vWF) is activated by high shear rates at sites of vascular narrowing or injury. A conformational change in the vWF molecule exposes the A1 loop, which binds to platelet membrane glycoprotein Ibα (GpIbα); vWF that is bound to the platelet membrane provides a bridge between the platelet and the subendothelial collagen matrix, which results in platelet adhesion. Activated vWF is cleaved by the ADAMTS13 protease, but does another molecule mediate the vWF-platelet interaction as well?
In a series of elegant experiments, investigators from the Netherlands studied the prothrombotic effects of plasma from patients who had antiphospholipid antibody syndrome (APS). Autoantibodies …