VWF deficiency and neutralization of VWF in Adamts13^−/−mice enhance neovascularization and decrease vascular damage. (A) Plasma VWF multimers from WT and Adamts13^−/− mice were determined using agarose gel electrophoresis and western blotting. (Bottom) Quantitative analysis of the ratio of ultralarge (UL) to low-molecular-weight (LMW) VWF multimers in each group. Values are mean ± SD. Unpaired, 2-tailed Student t test. n = 4 per group, *P < .05. (B) Representative images of CD31⁺ microvessels at 14 days after stroke in WT, Adamts13^−/−, Adamts13^−/−Vwf^−/−, Vwf^−/− mice, and Adamts13^−/− mice treated with the anti-VWF antibody, and quantification of percent area occupied by vascular structures for each group. (C) Representative images of multiphoton microscopy of IV injected FITC-dextran (MW = 2 000 000 Da) at 14 days after stroke in WT, Adamts13^−/−, Adamts13^−/−Vwf^−/−, Vwf^−/− mice, and Adamts13^−/− mice treated with the anti-VWF antibody, and quantification of perfused capillary length for each group. (D) Representative images and quantification of CD13⁺ pericyte coverage on CD31⁺ microvessels at 14 days after stroke in WT, Adamts13^−/−, Adamts13^−/−Vwf^−/−, Vwf^−/− mice, and Adamts13^−/− mice treated with the anti-VWF antibody. (E) Representative images of IgG deposits and CD31⁺ microvessels at 14 days after stroke in WT, Adamts13^−/−, Adamts13^−/−Vwf^−/−, Vwf^−/− mice, and Adamts13^−/− mice treated with the anti-VWF antibody, and quantification of extravascular IgG deposits for each group. Scale bars = 50 μm (B-D) and 10 μm (E). Values are mean ± SD. One-way ANOVA followed by Bonferroni multiple comparison test. n = 6 per group, *P < .05, ^#P < .05 compared with WT. NS, not significant.