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. 2012 Aug 1;7(8):e40222. doi: 10.1371/journal.pone.0040222

Figure 5. Laropiprant antagonizes the P-selectin expression and GPIIb/IIIa activation induced by TP and EP3 receptor activation. (A).

Figure 5

ADP (3 μmol/L) increased the surface expression of P-selectin in platelets primed with cytochalasin B (5 μg/mL), detected using a CD62P antibody. The EP3 agonist sulprostone (300 nmol/L) and U46619 (300 nmol/L) elevated P-selectin expression on the surface of platelets. These effects were counteracted by laropiprant at 10 μmol/L (n = 5). (B) The ADP (3 μmol/L) induced activation of GPIIb/IIIa, detected using a conformation-dependent antibody, PAC-1, was increased by sulprostone (300 nmol/L) and U46619 (300 nmol/L). Laropiprant at 10 µmol/L antagonized these effects (n = 5). (C) GPIIb expression was determined using an anti-CD41 antibody by flow cytometry. None of the treatments affected the GPIIb expression (n = 5). Data were expressed as percentage of ADP control response and are shown as mean+SEM. *P<0.05 as compared to vehicle and # P<0.05 as compared to the respective agonist treatment.