Figure 6.
In vitro and in vivo indicators of premature platelet activation. (A) Platelet counts in WT, RGS18−/−, RGS10−/−, and RGS10−/−18−/− mice treated daily for 10 days with 50 mg/kg aspirin (ASA; cyclooxygenase inhibitor) and 1.875 mg/kg prasugrel (pras; P2Y12 inhibitor) by oral gavage, followed by 5 days without treatment. n = 4; mean ± SEM. *P ≤ .05 for WT and RGS10−/− vs RGS18−/− vs RGS10−/−RGS18−/−. #P ≤ .05 for WT and RGS10−/− vs RGS18−/− and RGS10−/−RGS18−/−. Data showing the impact of these drugs on platelet activation is included in supplemental Figure 4. (B-C) Flow cytometric analysis of anti-TLT-1 binding (B) and TO staining (C) prior to and 5 days after drug treatment.

In vitro and in vivo indicators of premature platelet activation. (A) Platelet counts in WT, RGS18−/−, RGS10−/−, and RGS10−/−18−/− mice treated daily for 10 days with 50 mg/kg aspirin (ASA; cyclooxygenase inhibitor) and 1.875 mg/kg prasugrel (pras; P2Y12 inhibitor) by oral gavage, followed by 5 days without treatment. n = 4; mean ± SEM. *P ≤ .05 for WT and RGS10−/− vs RGS18−/− vs RGS10−/−RGS18−/−. #P ≤ .05 for WT and RGS10−/− vs RGS18−/− and RGS10−/−RGS18−/−. Data showing the impact of these drugs on platelet activation is included in supplemental Figure 4. (B-C) Flow cytometric analysis of anti-TLT-1 binding (B) and TO staining (C) prior to and 5 days after drug treatment.

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