Figure 2
Figure 2. Kindlin-2+/− ECs show enhanced inhibition of platelet aggregation. (A) Representative tracings of platelet aggregation induced by ADP (10 μM) in the absence or presence of increasing numbers of WT or kindlin-2+/− ECs. Under the same conditions, thrombin (0.5 U/mL) induced 100% aggregation. (B) ADP-induced aggregation of WT and kindlin-2+/− platelets in the presence of WT or kindlin-2+/− ECs. The percentage of aggregated platelets was determined 4 minutes after addition of ADP. Data are mean ± SEM (n = 9) and are representative of 3 independent experiments. (C) Effect of WT and kindlin-2+/− ECs on aggregation of WT platelets induced by collagen (1 and 2 μg/mL) or thrombin (0.05 and 0.5 U/mL). Data show the percentage of aggregated platelets 5 minutes after agonist addition and are means ± SEM (n = 3) from 2 independent experiments.

Kindlin-2+/ECs show enhanced inhibition of platelet aggregation. (A) Representative tracings of platelet aggregation induced by ADP (10 μM) in the absence or presence of increasing numbers of WT or kindlin-2+/− ECs. Under the same conditions, thrombin (0.5 U/mL) induced 100% aggregation. (B) ADP-induced aggregation of WT and kindlin-2+/− platelets in the presence of WT or kindlin-2+/− ECs. The percentage of aggregated platelets was determined 4 minutes after addition of ADP. Data are mean ± SEM (n = 9) and are representative of 3 independent experiments. (C) Effect of WT and kindlin-2+/− ECs on aggregation of WT platelets induced by collagen (1 and 2 μg/mL) or thrombin (0.05 and 0.5 U/mL). Data show the percentage of aggregated platelets 5 minutes after agonist addition and are means ± SEM (n = 3) from 2 independent experiments.

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