Platelet-derived VWF contributes to ischemic brain injury by promoting intracerebral thrombosis. Transient focal cerebral ischemia was induced by 60 minutes occlusion of the right middle cerebral artery, followed by 23 hours of reperfusion in WT (n = 9), VWF KO (n = 8), nontreated VWF PLT chimeric (n = 7), anti-GPIbα Fab-treated VWF PLT chimeric (p0p/B, n = 5), and control IgG Fab-treated VWF PLT chimeric (IgG Fab; n = 6) mice. Twenty-four hours after induction of ischemia, the amount of fibrin(ogen) in both the contralateral and ipsilateral hemisphere was determined by semiquantitative western blot analysis. (A) Representative immunoblot showing accumulation of fibrin(ogen) in ipsilateral (I) and contralateral (C) hemispheres. (B) Band intensities from A were quantified by densitometry. Each fibrin(ogen) density signal was first normalized to the corresponding actin density signal. The ratio of the normalized ipsilateral fibrin(ogen) density relative to the normalized contralateral fibrin(ogen) band served as a measurement for relative fibrin(ogen) deposition (ratio ipsilateral/contralateral [ratio IPSI/CONTRA]). ns, not statistically significant. *P < .05; **P < .01; ***P < .001.