Figure 6
Figure 6. Inhibition of platelet aggregation by OxHDL in eNOS−/−, Akt-1−/−, and Akt-2−/− platelets. Platelets prepared from eNOS−/− (A), Akt-1−/− (B), or Akt-2−/− (C) mice by gel filtration were preincubated with or without SR-BI blocking antibody, followed by incubation with 200 μg/mL murine OxHDL for 5 minutes at 37°C and stimulation with 0.1 U/mL thrombin. Platelet aggregation was monitored. (D) Data from panels A-C are presented as means plus or minus SD of 3 independent experiments. (E) Human platelets isolated by gel filtration were incubated with 200 μg/mL human OxHDL for 5 minutes at 37°C and stimulated with either 0.1 U/mL thrombin or 100 nM PMA. Platelet aggregation was monitored. (F) Data from panel E are presented as means plus or minus SD of 3 independent experiments. NA indicates no addition; α-SR-BI, anti–SR-BI blocking antibody. *P < .005; **P < .001.

Inhibition of platelet aggregation by OxHDL in eNOS−/−, Akt-1−/−, and Akt-2−/− platelets. Platelets prepared from eNOS−/− (A), Akt-1−/− (B), or Akt-2−/− (C) mice by gel filtration were preincubated with or without SR-BI blocking antibody, followed by incubation with 200 μg/mL murine OxHDL for 5 minutes at 37°C and stimulation with 0.1 U/mL thrombin. Platelet aggregation was monitored. (D) Data from panels A-C are presented as means plus or minus SD of 3 independent experiments. (E) Human platelets isolated by gel filtration were incubated with 200 μg/mL human OxHDL for 5 minutes at 37°C and stimulated with either 0.1 U/mL thrombin or 100 nM PMA. Platelet aggregation was monitored. (F) Data from panel E are presented as means plus or minus SD of 3 independent experiments. NA indicates no addition; α-SR-BI, anti–SR-BI blocking antibody. *P < .005; **P < .001.

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