Reduced platelet deposition to the ligation injured carotid artery in Tlr2-deficient mice is independent of the platelet genotype, and the adhesion defect is rescued by VWF supplementation. (A) Imaging of DCF, 5- (and 6) carboxy-2’,7’-dichlorofluorescein diacetate (carboxy-DCFDA)-stained platelet deposits (green) to the ligation-injured common carotid artery in WT (top) and Tlr2^−/− (bottom) mice 30 minutes after transient ligation; representative images and quantification (8-11 mice per group). (B) Representative images of DCF-stained platelet deposits (green) to the ligation-injured common carotid artery in WT (top) and Tlr2^−/− (bottom) mice 5 minutes after transient ligation. (C) Platelet deposition in hGPIbα mice after platelet depletion and reconstitution with DCF stained WT (top) or Tlr2^−/− platelets (bottom) 30 minutes after transient ligation; representative images and quantification (10 mice per group). (D) Imaging of DCF-stained platelet deposits (green) to the ligation-injured common carotid artery in WT and Tlr2^−/− mice treated with sodium chloride (vehicle) or 153 mIU human VWF (Wilfactin) per mouse (6-10 mice per group). Scale bar, 200 µm. Representative images are shown. Mean ± SEM; repeated measurement ANOVA (mixed model), *P < .05. n.s., not significant.