Figure 1.
Figure 1. Aggregation of αIIbβ3-deficient or αIIbβ3-inhibited platelets by rFVIIa-mediated fibrin formation. Washed platelets from a patient with GT (A) or platelets from healthy volunteers pretreated with dRGDW for 5 minutes (200 μM; B-C) were activated with collagen (4 μg/mL; A-B) or TRAP (15 μM; C), a mixture of factors VIIa (1.2 μg/mL), X (10 μg/mL), II (20 ng/mL), and fibrinogen (0.5 mg/mL), or with collagen or TRAP in combination with the coagulation factors, all in the presence of 3 mM CaCl2. Platelet aggregation was monitored using standard suspension aggregometry at 37°C using a stir speed of 900 rpm. In panels B and C, aggregation of washed platelets with collagen or TRAP in the absence of dRGDW is shown for reference. Panel A is a typical representation of experiments with 3 unrelated GT patients; panels B and C represent a typical representation of more than 10 experiments.

Aggregation of αIIbβ3-deficient or αIIbβ3-inhibited platelets by rFVIIa-mediated fibrin formation. Washed platelets from a patient with GT (A) or platelets from healthy volunteers pretreated with dRGDW for 5 minutes (200 μM; B-C) were activated with collagen (4 μg/mL; A-B) or TRAP (15 μM; C), a mixture of factors VIIa (1.2 μg/mL), X (10 μg/mL), II (20 ng/mL), and fibrinogen (0.5 mg/mL), or with collagen or TRAP in combination with the coagulation factors, all in the presence of 3 mM CaCl2. Platelet aggregation was monitored using standard suspension aggregometry at 37°C using a stir speed of 900 rpm. In panels B and C, aggregation of washed platelets with collagen or TRAP in the absence of dRGDW is shown for reference. Panel A is a typical representation of experiments with 3 unrelated GT patients; panels B and C represent a typical representation of more than 10 experiments.

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