Figure 6.
Figure 6. Effect of inhibitors on PAR-mediated thromboxane A2 generation and dense granule release in human platelets. Washed platelets without aspirin treatment were stimulated with SFLLRN or AYPGKF in the presence or absence of 5μM Rottlerin (A) or with SFLLRN in the presence of different concentrations of PP2 (B) at 37°C, and the generated thromboxane B2 was measured as described in “Results” by ELISA. Washed and aspirin-treated human platelets were stimulated with different concentrations of SFLLRN (C) or AYPGKF (D) in the presence of 10 μM PP2 (broken lines) or 10 μM PP3 (solid lines), and the dense granule secretion was measured using Lumichrome reagent. The mean ± SD is derived from experiments performed using platelets obtained from 3 independent donors.

Effect of inhibitors on PAR-mediated thromboxane A2 generation and dense granule release in human platelets. Washed platelets without aspirin treatment were stimulated with SFLLRN or AYPGKF in the presence or absence of 5μM Rottlerin (A) or with SFLLRN in the presence of different concentrations of PP2 (B) at 37°C, and the generated thromboxane B2 was measured as described in “Results” by ELISA. Washed and aspirin-treated human platelets were stimulated with different concentrations of SFLLRN (C) or AYPGKF (D) in the presence of 10 μM PP2 (broken lines) or 10 μM PP3 (solid lines), and the dense granule secretion was measured using Lumichrome reagent. The mean ± SD is derived from experiments performed using platelets obtained from 3 independent donors.

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