Figure 2.

Cav-1 deficiency exacerbates the formation of microvascular thrombi 24 h after cerebral I/R injury. (a, c) Representative confocal images of thrombocytes (red) and fibrinogen (red) in the CD31⁺ cerebral microvessels (green) in the peri-infarct area from WT and Cav-1^−/− mice 24 h after tMCAO [quantified in (b, d); n = 6 in each group; mean ± S.D; **P < 0.01 vs. WT tMCAO mice by unpaired t-test]. (e, f) HE staining and quantification showing occluded microvessels (indicated by black arrowheads) 24 h after the surgery. Results are expressed as the number of occluded vessels relative to the area (n = 6 in each group; mean ± S.D; *P < 0.05 vs. WT tMCAO mice by unpaired t-test). (g, h) Representative images of immunofluorescence staining and quantification of FITC-dextran perfusion in the CD31⁺ cerebral microvessels (red) 24 h post-stroke. Data are presented as the percentage of perfusion vessels relative to the area (n = 6 in each group; mean ± S.D; **P < 0.01 vs. WT tMCAO mice by unpaired t-test). (i–k) Immunoblotting and quantification showing the expression of vWF and PAI-1 in brain microvessels from the peri-infarct region 24 h post-tMCAO (a pool of 2 mice per sample, n = 5 samples in each group; mean ± S.D; **P < 0.01 vs. WT tMCAO mice by unpaired t-test). Scale bar: 20 μm. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)