Intravascular ERp72 is required for platelet accumulation and fibrin formation in vivo. (A-C) Cremaster arteriole injury was induced in Pf4-Cre/ERp72^fl/fl mice and their Cre-negative ERp72^fl/fl littermate control mice. Platelets and fibrin accumulated at the site of injury were detected using anti-CD41 F(ab)₂ fragments conjugated to Alexa Fluor 488 and anti–fibrin antibody conjugated to Alexa Fluor 647. (A) Representative fluorescence images in intravital microscopy for platelet accumulation (green) and fibrin deposition (red) at the indicated time points after injury . Original magnification ×64. Scale bar, 30 μm. The median integrated fluorescence intensities (FIs) of anti-CD41 (platelet, B) and anti–fibrin (fibrin, C) antibodies over 300 seconds. (D-F) Cremaster arteriole injury was induced in Tie2-Cre/ERp72^fl/fl mice and Cre-negative ERp72^fl/fl littermate control mice. Tie2-Cre/ERp72^fl/fl mice were infused with ERp72(ss-ss-ss) or ERp72(oo-ss-ss) (150 μg/mouse). (D) Representative fluorescence images of platelet accumulation (green) and fibrin deposition (red). Original magnification ×64. Scale bar, 30 μm. The data of fluorescence intensities of anti–CD41 antibody (platelet, E) and anti–fibrin antibody (fibrin, F) were obtained from 30 thrombi in 3 mice. Fluorescence signal was not observed using fluorescently labeled control immunoglobulin G (not depicted). The area under the curve of fluorescence intensity over 300 seconds was analyzed using a Kruskal-Wallis test. Only significant differences are shown; *P < .05; ***P < .001. The data were obtained from 30 thrombi in 3 mice for each experimental condition.