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 Blood, 9 April 2009, Vol. 113, No. 15, pp. 3600-3603.
Prepublished online as a Blood First Edition Paper on January 30, 2009; DOI 10.1182/blood-2008-09-180695.

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THROMBOSIS AND HEMOSTASIS

Brief Report

Deficiency of von Willebrand factor protects mice from ischemic stroke

Christoph Kleinschnitz1, Simon F. De Meyer2, Tobias Schwarz1, Madeleine Austinat1, Karen Vanhoorelbeke2, Bernhard Nieswandt3,4, Hans Deckmyn2, and Guido Stoll1

1 Department of Neurology, University of Wuerzburg, Wuerzburg, Germany; 2 Laboratory for Thrombosis Research, KU Leuven Campus, Kortrijk, Belgium; and 3 Rudolf Virchow Center, Deutsche Forschungsgemeinschaft (DFG) Research Center for Experimental Biomedicine and 4 Institute of Clinical Biochemistry and Pathobiochemistry, University of Wuerzburg, Wuerzburg, Germany

We recently demonstrated that blockade of the platelet adhesion receptor glycoprotein (GP) Ib{alpha} protects mice from ischemic stroke. Although von Willebrand factor (VWF) is the major ligand for GPIb{alpha}, GPIb{alpha} can engage other counterreceptors on endothelial cells, platelets, and leukocytes (eg, Mac-1 or P-selectin) potentially involved in stroke outcome. To further analyze whether VWF is of particular relevance for stroke development, VWF–/– mice underwent 60 minutes of middle cerebral artery occlusion. After 24 hours, VWF–/– mice had significantly smaller infarctions (P < .05) and less severe neurologic deficits (P < .01) compared with controls. This effect was sustained after 1 week, and intracranial bleeding was absent in VWF–/– mice as revealed by serial magnetic resonance imaging. Hydrodynamic injection of a VWF-encoding plasmid restored the susceptibility for stroke in VWF–/– mice. This study indicates that VWF is critically involved in cerebral ischemia. Hence, targeted inhibition of the GPIb{alpha}-VWF pathway might become a promising therapeutic option.


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