Fig. 4.
Fig. 4. The role of thrombin, PAR-1, and plasminogen in Sk-induced platelet aggregation. / Aggregations to ADP and Sk (A) or 0.35 U/mL thrombin (B) were performed without inhibitors or in the presence of the PAR-1-blocking antibody 2/389 (4 μg/mL), hirudin (1 U/mL), or the thrombin active site inhibitor Ro46-6240 (Ro-46) (0.04 μg/mL). (C) Aggregation to ADP and Sk was performed in PRP depleted of plasminogen by passage over a lysine-Sepharose column, to which had been added buffer alone, wild-type plasminogen, or the inactive mutant S741A plasminogen. Each tracing is representative of 2 to 3 experiments.

The role of thrombin, PAR-1, and plasminogen in Sk-induced platelet aggregation.

Aggregations to ADP and Sk (A) or 0.35 U/mL thrombin (B) were performed without inhibitors or in the presence of the PAR-1-blocking antibody 2/389 (4 μg/mL), hirudin (1 U/mL), or the thrombin active site inhibitor Ro46-6240 (Ro-46) (0.04 μg/mL). (C) Aggregation to ADP and Sk was performed in PRP depleted of plasminogen by passage over a lysine-Sepharose column, to which had been added buffer alone, wild-type plasminogen, or the inactive mutant S741A plasminogen. Each tracing is representative of 2 to 3 experiments.

Close Modal

or Create an Account

Close Modal
Close Modal