Loss of PITP in platelets impairs thrombin generation and Annexin V binding. (A-D) Representative kinetics of thrombin generation induced by BF610 tumor cells (A,B) or TF (C,D) in platelet-rich plasma (PRP) from Pitpβ^fl/flPf4-Cre^- mice (wild-type control, navy trace), Pitpβ^fl/flPf4-Cre⁺ mice (PITPβ-null, red trace), and Pitpα^fl/fl/β^fl/flPf4-Cre⁺ mice (PITPα/β-null, purple trace). Endogenous thrombin potential is shown as the mean value of total thrombin induced by B16F10 tumor cells (B) or by TF (D) over 90 minutes of reaction time in PRP containing PITPβ-null platelets (red bars), PITPα/β-null platelets (purple bars), and their wild-type controls (navy bars). (E,F) Platelet-poor plasma (PPP) was used as a control to demonstrate the platelet-intrinsic nature of thrombin generation upon stimulation with B16F10 tumor cells (E) or TF (F). n = 3 mice per group. Statistical analysis was performed using an unpaired t test. Error bars are s.d. (G) Platelets lacking PITPβ and both PITP isoforms have an impaired ability to bind Annexin V after activation by the combination of 5 μg/mL collagen and 0.05 U/mL thrombin. The mean values are averaged from 4 independent experiments. Data were analyzed using unpaired t test. Error bars are s.d.