Hemostasis and platelet function is unaltered by the absence ofcaspase-9. (A) Caspase-9 is not essential for normal platelet activation in vitro. Washed platelets were stimulated in vitro with activation agonists. The cell-surface profile of platelets was examined by measuring the platelet activation markers P-selectin, integrin GpIIb/IIIa, and PS exposure by flow cytometry. Data represent the mean ± SD; n = 4-5 mice per genotype (except Thr. [0.5 U/mL] + Conv. [500 ng/mL], n = 2). (B) Platelet aggregation kinetics is not altered by the absence of caspase-9. Aggregation of washed platelets derived from Casp9^+/+ and Casp9^−/− FLC-reconstituted mice was measured using an aggregometer. Data represent the mean ± SD; n > 3 mice/genotype per condition (except ADP 5.0μM, n = 2). (C) Loss of caspase-9 does not alter tail-bleeding time. Bleeding time was measured using the template method. Data represent the mean ± SEM; n = 5-7 mice per gentoype. (D) Template tail-bleeding time following administration of hirudin anticoagulant. Data represent the mean ± SEM; n = 6-8 mice per gentoype. (E) Bleeding time of transected tail. Data represent the mean ± SEM; n = 5-6 mice per genotype.