The thrombotic platelet receptor GPVI is more active in human patients with AAA. Platelets from control patients (n = 5) and patients with AAA (n = 4) were analyzed for the platelet receptor GPVI. Platelet GPVI, platelet factor 4 (PF4), and CD42a protein expression was measured by western blot (A) and quantified by densitometry (B-D). GPVI on the platelet surface is increased in patients with AAA vs control (E) as demonstrated by platelet surface flow cytometry (∗P = .039 by Student t test). (F) Platelets isolated from patients with AAA demonstrated significantly more surface P-selectin in response to the GPVI specific agonist convulxin than control as measured by flow cytometry (∗P = .046; ∗∗∗P < .001, patients with AAA vs control patients by 2-way ANOVA). Data are represented as individual points or mean ± standard error of the mean (SEM). MFI, mean fluorescence intensity; n.s, not significant.
Figure 2.

The thrombotic platelet receptor GPVI is more active in human patients with AAA. Platelets from control patients (n = 5) and patients with AAA (n = 4) were analyzed for the platelet receptor GPVI. Platelet GPVI, platelet factor 4 (PF4), and CD42a protein expression was measured by western blot (A) and quantified by densitometry (B-D). GPVI on the platelet surface is increased in patients with AAA vs control (E) as demonstrated by platelet surface flow cytometry (∗P = .039 by Student t test). (F) Platelets isolated from patients with AAA demonstrated significantly more surface P-selectin in response to the GPVI specific agonist convulxin than control as measured by flow cytometry (∗P = .046; ∗∗∗P < .001, patients with AAA vs control patients by 2-way ANOVA). Data are represented as individual points or mean ± standard error of the mean (SEM). MFI, mean fluorescence intensity; n.s, not significant.

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