GPVI blockade via intervention with JAQ1 antibody blunts AngII–induced AAA expansion and rupture-induced death. (A) Study schematic. Male Ldlr^−/− mice (aged 8-10 weeks) were infused with AngII (1000 ng/kg per day) via osmotic pump implantation. After 14 days of AngII infusion, mice were blindly randomized into 2 groups of controlled for aortic diameter and given either a 1-time IP injection of 50-μg JAQ1 antibody (n = 9) or 50-μg IgG control (n = 9). After another 14 days, mice were euthanized, final aortic diameter was measured ex vivo, and tissues were harvested for further analysis. (B) Intraluminal aortic diameters measured by weekly ultrasound (∗∗∗P < .001, JAQ1 vs control by 2-way repeated measures ANOVA). (C) Aortic diameters in JAQ1-treated vs control-treated mice measured ex vivo 28 days after AngII infusion (∗P = .045 by Student t test). (D) Representative images of aortas ex vivo from the indicated groups. Platelet activation measured 14 days after JAQ1 or IgG antibody intervention indicated by surface P-selectin (FITC) levels in response to varying doses of the GPVI specific agonist convulxin (E) or thrombin (F) in JAQ1-treated vs control mice measured flow cytometry (n = 6 per group; ∗P = .032; ∗∗P = .01; ∗∗∗P < .001, JAQ1 vs control by 2-way ANOVA). (G) Representative flow cytometry scatterplots from the indicated conditions. Data are represented as individual data points or mean ± SEM. IP, intraperitoneal.