Binding of von Willebrand factor to collagen and glycoprotein Ibalpha, but not to glycoprotein IIb/IIIa, contributes to ischemic stroke in mice--brief report.
Laboratory for Thrombosis Research, KULeuven Campus Kortrijk, E Sabbelaan 53, B-8500 Kortrijk, Belgium.
Journal Article: Arteriosclerosis Thrombosis and Vascular Biology (impact factor: 7.24). 10/2010; 30(10):1949-51. DOI: 10.1161/ATVBAHA.110.208918
Abstract
VWF(-/-) mice received gene transfer to express mutants of VWF defective either in binding to fibrillar collagen, glycoprotein (GP)Ibα or GPIIb/IIIa, and underwent 60 minutes of transient middle cerebral artery occlusion. In VWF(-/-) mice reconstituted with VWF mutants defective in binding to collagen or GPIbα, protection against stroke was sustained, whereas VWF lacking the GPIIb/IIIa binding site restored full susceptibility similar to normal VWF.
VWF-collagen and VWF-GPIbα (but not VWF-GPIIb/IIIa) interactions are instrumental in thrombus formation after transient middle cerebral artery occlusion, and their inhibition could be a promising target for stroke treatment.
Source: PubMed
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