Figure 3.
MPαC-induced platelet activation depends on PKC. (A-E) The effect of the pan-PKC inhibitor Gö6983 on (A) MPαC-induced washed human platelet aggregation (n = 4 independent experiments), (B) PAC-1 binding, (C) P-selectin exposure, (D) ATP release, (E) and PS externalization (n = 5 independent experiments). (F) MPαC-induced P-selectin exposure, (G) JON/A (a monoclonal antibody against activated mouse integrin αIIbβ3) binding, and (H) PS externalization on washed WT and Prkca−/− platelets (n = 8 mice per genotype). One-way ANOVA followed by Dunnett post hoc test in panels A-E; 2-tailed Student t test in panels F-H. Data are shown as mean ± SEM for panels A-H. ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001.

MPαC-induced platelet activation depends on PKC. (A-E) The effect of the pan-PKC inhibitor Gö6983 on (A) MPαC-induced washed human platelet aggregation (n = 4 independent experiments), (B) PAC-1 binding, (C) P-selectin exposure, (D) ATP release, (E) and PS externalization (n = 5 independent experiments). (F) MPαC-induced P-selectin exposure, (G) JON/A (a monoclonal antibody against activated mouse integrin αIIbβ3) binding, and (H) PS externalization on washed WT and Prkca−/− platelets (n = 8 mice per genotype). One-way ANOVA followed by Dunnett post hoc test in panels A-E; 2-tailed Student t test in panels F-H. Data are shown as mean ± SEM for panels A-H. ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001.

Close Modal

or Create an Account

Close Modal
Close Modal