SR-BI deficiency modulates platelet integrin α_IIbβ₃ activation and P-selectin expression in the absence of changes in platelet expression of major receptors. (A-B) Platelets in PRP from WT and SR-BI^−/− mice were stimulated with selective protease-activated receptor 4–activating peptides (PAR4-AP), ADP, or convulxin (CVX). Platelet integrin α_IIbβ₃ activation and P-selectin (CD62) expression were determined using the PE-conjugated antibody for murine α_IIbβ₃ in the activated conformation (JON/A) or murine P-selectin. (C) Platelets were isolated by gel filtration from mice of indicated genotypes, and activation of integrin α_IIbβ₃ was assessed by FACS analysis. (A) Flow cytometry histograms from representative experiments are shown. (B-C) Quantification of FACS analysis data presented as mean ± SEM of at least 3 independent experiments. *P < .05, **P < .01. (D) Expression of thrombin receptors PAR4 and PAR3 and ADP receptors P2Y1 and P2Y12 were assessed by Western blotting. (E) Expression of collagen receptor GPVI and α_IIbβ₃ integrin. Platelets were incubated with FITC-labeled anti-α_IIbβ₃ or anti-GPVI antibody and analyzed by flow cytometry. Data are presented as mean ± SEM of at least 4 independent experiments.