Fig. 1.
ADP- and TxA2-induced signaling is required to cause aggregation in response to a low concentration of collagen.
Wild-type (WT) or Tp-deficient (Tp−/−) platelets in plasma were activated with a low concentration (2.5 μg/mL) of collagen. Tp-deficient platelet aggregation was diminished and reversible (A), and ATP secretion and TxA2 production levels were substantially diminished in response to a low concentration of collagen (B). After preincubation with apyrase (10 U/mL), A3P5P (2mM), and AR-C69931MX (2 μM) for 3 minutes, wild-type and Tp-deficient platelets were activated with a low concentration (2.5 μg/mL) of collagen. Aggregation of both Tp-deficient and wild-type platelets was inhibited in response to a low concentration of collagen (C). TxA2 production from both Tp-deficient and wild-type platelets treated with apyrase, A3P5P, and AR-C69931MX were similar in response to a low concentration of collagen (D), although the level of TxA2 production was substantially less than in the platelets untreated with apyrase and the ADP receptor antagonists (B,D). Data were obtained from 6 tests. Bars represent means ± SEM.