Platelet- and VWF-mediated–collagen binding in a ferric chloride-induced cremasteric arteriolar injury model. (A) Impact of GPVI and α2β1 depletion in the ferric chloride injury model. Occlusion time course with the following mice: VWF^−/− expressing WT-mVWF, treated with JAQ1 (GPVI depletion) (n = 6), LEN/B (α2β1 depletion) (n = 9), and VWF^−/− mice treated with JAQ1 (n = 9) or both JAQ1 and LEN/B (n = 8). The impact of JAQ1 was similar to VWF^−/−. However, the combination of both did not demonstrate further inhibition. LEN/B-treated mice demonstrated a milder phenotype. Treatment of both JAQ1 and LEN/B in VWF^−/− mice markedly inhibited thrombus formation, although residual initial platelet adhesion was observed. (B) Summary of the extent of vessel occlusion in the intravital experiments. Box-and-whisker plots of occlusion extent for each injury condition. The extent of occlusion with each injury was defined as the integrated occlusion time course, determined by area under the curve using the trapezoidal rule. Median and interquartile range are shown. ***P < .001, ****P < .0001.