Figure 1.
Figure 1. Inhibition of IP in human platelets diminishes 12-HETrE antiplatelet effects PAR4-mediated platelet aggregation. The minimal concentration of PAR4-AP (25-50 µM) inducing full platelet aggregation (>70%) in DMSO-treated human platelets was used to stimulate platelets incubated with increasing concentrations of 12-HETrE (5-25 µM) in the presence of a vehicle control or an antagonist to IP (R03244794; 250 nM; n = 3-6) (A), EP2 (TG4-155; 2 μM) and EP4 (CJ-42794; 80 nM) (n = 5) (B), or DP1 (MK 0524; .4 nM; n = 5) (C). Two-way statistical analysis of variance was performed. Known antiplatelet prostanoid receptor agonists PGI2 (4 nM), PGE2 (20 μM), and PGD2 (30 nM) were used to confirm the efficacy of R03244794, TG4-155/CJ-42794, or MK 052480, respectively. Two-tailed, paired t test was performed; *P < .05, **P < .01, ***P < .001. Data represent mean ± standard deviation.

Inhibition of IP in human platelets diminishes 12-HETrE antiplatelet effects PAR4-mediated platelet aggregation. The minimal concentration of PAR4-AP (25-50 µM) inducing full platelet aggregation (>70%) in DMSO-treated human platelets was used to stimulate platelets incubated with increasing concentrations of 12-HETrE (5-25 µM) in the presence of a vehicle control or an antagonist to IP (R03244794; 250 nM; n = 3-6) (A), EP2 (TG4-155; 2 μM) and EP4 (CJ-42794; 80 nM) (n = 5) (B), or DP1 (MK 0524; .4 nM; n = 5) (C). Two-way statistical analysis of variance was performed. Known antiplatelet prostanoid receptor agonists PGI2 (4 nM), PGE2 (20 μM), and PGD2 (30 nM) were used to confirm the efficacy of R03244794, TG4-155/CJ-42794, or MK 052480, respectively. Two-tailed, paired t test was performed; *P < .05, **P < .01, ***P < .001. Data represent mean ± standard deviation.

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