Absence of PS expression in platelets affects resistance to APC- and TFPI-dependent PS activity. (A-B) APC-dependent activity assessed by thrombin generation in PRP (150 × 10⁹/L platelets). Representative thrombin generation curves in presence of different amount of WT mAPC and L38D mAPC or buffer (no APC) in PRP from Pros1^lox/loxPf4-Cre⁻ (A) and Pros1^lox/loxPf4-Cre⁺ mice (B). (C-D) Washed platelet suspension (150 G/L) from Pros1^lox/loxPf4-Cre⁻ (C) and Pros1^lox/loxPf4-Cre⁺ mice (D) were reconstituted in platelet-free plasma (PFP) from F8^−/−Pros1^−/− mice, lacking plasma PS to evaluate the contribution of platelet PS to APC activity. (E-F) To evaluate the contribution of platelet PS to the thrombin potential, thrombin generation was measured in Pros1^lox/loxPf4-Cre⁻ and Pros1^lox/loxPf4-Cre⁺ mice. ETP values from PRP (200 G/L platelets) (E) and PFP (F) are shown for both genotypes. (G) ETP change between PRP and PFP [(ETP_PRPx100/ETP_PFP)-100)] in Pros1^lox/loxPf4-Cre⁻ and Pros1^lox/loxPf4-Cre⁺ mice. Data are expressed as mean ± SEM. *P < .05; **P ≤ .01. (H) FXa in activated Pros1^lox/loxPf4-Cre⁻ and Pros1^lox/loxPf4-Cre⁺ platelets; representative experiment obtained from a pool of 5 to 6 mice/genotype.