The GPIb-VWF axis in experimental stroke development. In the postischemic cerebral microvasculature, UL-VWF released from activated or damaged endothelial cells and platelets promotes platelet recruitment and thrombus growth. In flowing blood, UL-VWF is cleaved by ADAMTS13 to smaller VWF multimers that are less adhesive and circulate in plasma. Absence of ADAMTS13 leads to increased thrombus formation and larger infarctions, whereas infusion of exogenous ADAMTS13 reduces thrombotic activity and infarct size. An even stronger inhibition of thrombotic activity and, consequently, markedly reduced infarct size is achieved by inhibition of GPIb or absence of VWF.