Figure 1.
Platelet-dependent prolongation of plasma clot lysis time (pCLT) determined by the turbidimetric method. A final concentration of 2 nM (A-B) or 1.5 nM/1.0 nM (C) tissue-type plasminogen activator (tPA). pCLTs are shown as the average ± standard deviation. (A) pCLT values at different concentrations of platelet-containing plasma. The number of samples is as follows; 0, 20, 40, 80, and 160 (× 109/L) platelets, n = 18, n = 14, n = 6, n = 17, and n = 10, respectively (9 independent experiments from 4 donors). (B) The involvement of the thrombomodulin (TM)/thrombin-activatable fibrinolysis inhibitor (TAFI) system in pCLT. Red (control), 0, 80, and 160 (× 109/L) platelets, n = 18, n = 17, and n = 10, respectively; blue (activated TAFI inhibitor [TAFIaI]), 0, 80, and 160 (× 109/L) platelets, n = 11, n = 11, and n = 8 respectively; and green (neutralizing antibody of TM [TM-Ab]), 0, 80, and 160 (× 109/L) platelets, n = 7, n = 7, and n = 6, respectively. The effects of TAFIaI were determined in the presence of 5 nM soluble TM, which potently activates TAFI, at different platelet concentrations. Red bars (control): 0, 80, and 160 (× 109/L) platelets, n = 8, n = 7, and n = 3, respectively. Blue bars (TAFIaI): 0, 80, and 160 (× 109/L) platelets, n = 5, n = 6, and n = 3, respectively. (C) Requirement for TAFI in plasma for the platelet-dependent prolongation of pCLT. The number of samples was the same in each group; normal plasma and TAFI-deficient plasma (tPA 1.5 nM, tPA 1.0 nM), n = 5, n = 4, and n = 7, respectively. Red bars are control and blue bars are TAFIaI. Data were analyzed as follows: Williams multiple comparison test: *P < .05 (TM), **P < .01, Welch’s t test: #P < .005 vs control, ##P < .001 vs control; Student t test: +P < .005, ++P < .001 vs control.

Platelet-dependent prolongation of plasma clot lysis time (pCLT) determined by the turbidimetric method. A final concentration of 2 nM (A-B) or 1.5 nM/1.0 nM (C) tissue-type plasminogen activator (tPA). pCLTs are shown as the average ± standard deviation. (A) pCLT values at different concentrations of platelet-containing plasma. The number of samples is as follows; 0, 20, 40, 80, and 160 (× 109/L) platelets, n = 18, n = 14, n = 6, n = 17, and n = 10, respectively (9 independent experiments from 4 donors). (B) The involvement of the thrombomodulin (TM)/thrombin-activatable fibrinolysis inhibitor (TAFI) system in pCLT. Red (control), 0, 80, and 160 (× 109/L) platelets, n = 18, n = 17, and n = 10, respectively; blue (activated TAFI inhibitor [TAFIaI]), 0, 80, and 160 (× 109/L) platelets, n = 11, n = 11, and n = 8 respectively; and green (neutralizing antibody of TM [TM-Ab]), 0, 80, and 160 (× 109/L) platelets, n = 7, n = 7, and n = 6, respectively. The effects of TAFIaI were determined in the presence of 5 nM soluble TM, which potently activates TAFI, at different platelet concentrations. Red bars (control): 0, 80, and 160 (× 109/L) platelets, n = 8, n = 7, and n = 3, respectively. Blue bars (TAFIaI): 0, 80, and 160 (× 109/L) platelets, n = 5, n = 6, and n = 3, respectively. (C) Requirement for TAFI in plasma for the platelet-dependent prolongation of pCLT. The number of samples was the same in each group; normal plasma and TAFI-deficient plasma (tPA 1.5 nM, tPA 1.0 nM), n = 5, n = 4, and n = 7, respectively. Red bars are control and blue bars are TAFIaI. Data were analyzed as follows: Williams multiple comparison test: *P < .05 (TM), **P < .01, Welch’s t test: #P < .005 vs control, ##P < .001 vs control; Student t test: +P < .005, ++P < .001 vs control.

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