Figure 1
Figure 1. CAP-PEs induce platelet activation. (A-D) Human platelets were isolated by gel filtration and were incubated with indicated agonists (A,C) CEP-PE (10 μM), PE (10 μM), ADP (10 μM), thrombin (Thr; 0.05 U/mL), and (B,D) CHP-PE (10 μM). Then, P-selectin (A-B) expression or integrin αIIbβ3 (C-D) activation was assessed by FACS analysis. (E, F) Murine platelets were isolated by gel filtration and incubated with (E) CEP-PE (20 μM), (F) CHP-PE (20 μM), or control agonists including PE (20 μM), ADP (10 μM), or thrombin (0.05 U/mL). Integrin αIIbβ3 activation was assessed by FACS analysis. (Left) Histogram presentations of FACS analysis data; (right) quantification data (means ± SD) from 3 independent experiments. ***P < .001 vs resting platelets.

CAP-PEs induce platelet activation. (A-D) Human platelets were isolated by gel filtration and were incubated with indicated agonists (A,C) CEP-PE (10 μM), PE (10 μM), ADP (10 μM), thrombin (Thr; 0.05 U/mL), and (B,D) CHP-PE (10 μM). Then, P-selectin (A-B) expression or integrin αIIbβ3 (C-D) activation was assessed by FACS analysis. (E, F) Murine platelets were isolated by gel filtration and incubated with (E) CEP-PE (20 μM), (F) CHP-PE (20 μM), or control agonists including PE (20 μM), ADP (10 μM), or thrombin (0.05 U/mL). Integrin αIIbβ3 activation was assessed by FACS analysis. (Left) Histogram presentations of FACS analysis data; (right) quantification data (means ± SD) from 3 independent experiments. ***P < .001 vs resting platelets.

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