Fig. 3.
Fig. 3. Effects of TSP2 deficiency on platelet aggregation. / (A) PRP (1 × 108 platelets/mL) from wild-type (●) and TSP2-null (○) mice was treated with ADP (10 μm), and the aggregation response was monitored by a change in transmittance. The aggregation of wild-type platelets was set at 90% to correct for the background signal obtained with platelet-poor plasma. The results are the average of 3 independent experiments. (B) Representative tracings of the aggregation responses of TSP2-null washed platelets (1 × 108/mL) to thrombin (1 U/mL), collagen (10 μg/mL), and ADP (10 μm) are shown. For the latter a representative tracing of the aggregation response of wild-type platelets (WT) is also shown. A total of 5 mice per genotype was used to generate washed platelets, and each experiment was repeated 4 times. (C) Representative tracings of ATP secretion from ADP-activated blood samples from wild-type (WT) and TSP2-null (KO) mice. The experiment was repeated twice.

Effects of TSP2 deficiency on platelet aggregation.

(A) PRP (1 × 108 platelets/mL) from wild-type (●) and TSP2-null (○) mice was treated with ADP (10 μm), and the aggregation response was monitored by a change in transmittance. The aggregation of wild-type platelets was set at 90% to correct for the background signal obtained with platelet-poor plasma. The results are the average of 3 independent experiments. (B) Representative tracings of the aggregation responses of TSP2-null washed platelets (1 × 108/mL) to thrombin (1 U/mL), collagen (10 μg/mL), and ADP (10 μm) are shown. For the latter a representative tracing of the aggregation response of wild-type platelets (WT) is also shown. A total of 5 mice per genotype was used to generate washed platelets, and each experiment was repeated 4 times. (C) Representative tracings of ATP secretion from ADP-activated blood samples from wild-type (WT) and TSP2-null (KO) mice. The experiment was repeated twice.

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