oxLDL inhibits cGMP-signaling through a mechanism that requires NOX2 and intracellular ROS. (A) Platelets (5 × 10⁸ platelets/mL) were incubated with apyrase (2 U/mL), indomethacin (10 µmol/L), and EGTA (1 mmol/L) and treated with MnTMPyP (100 µmol/L) or TEMPOL (1 mmol/L) prior to the addition of 8-pCPT-cGMP (50 µmol/L) for 2 minutes. Platelets were lysed, separated by SDS-PAGE, and immunoblotted (IB) for phospho–VASP-ser²³⁹. (i) Blots are representative of at least 3 experiments using different blood donors. (ii) Densitometric analysis of the blots. **P < .01 compared with the absence of inhibitors. (B) As in panel A, except that in some cases, platelets were pretreated with gp91ds-tat or its scrambled control (both 2 µmol/L). Blots are representative of at least 3 separate experiments. *P < .05 for CGMP alone, cGMP/oxLDL, and oxLDL in the presence and absence of gp91da-tat. (C) As in panel A, except NOX2-deficient or WT murine platelets were treated with 8pCPT-cGMP (50 µmol/L) and oxPC_CD36 (5 µmol/L). *P < .05 compared with the absence of oxPC_CD36. NS, not significant.