Figure 7.
Inhibiting the proximal steps in the complement pathway impairs platelet adhesion to human umbilical vein endothelial cells induced by KKO. Microfluidic channels coated with human umbilical vein endothelial cells were perfused with recalcified citrated WB stimulated with monoclonal Ab KKO (50 µg/mL) in the presence of PF4 (25 µg/mL). Some samples were preincubated with C1r inhibitor [C1r(i); 5 µg/mL, 25 µg/mL, or 100 µg/mL] 15 minutes before the addition of KKO (50 µg/mL) and PF4 (25 µg/mL). Adhesion of calcein-labeled platelets was measured as total fluorescent intensity at 5-minute intervals, and the effect of C1r(i) is expressed as percentage of platelet adhesion in the presence of inhibitor compared with platelet adhesion without inhibitor (100%). *P < .05, **P < .005, ***P < .0005 (2-way analysis of variance with Dunnett’s correction); n = 4.

Inhibiting the proximal steps in the complement pathway impairs platelet adhesion to human umbilical vein endothelial cells induced by KKO. Microfluidic channels coated with human umbilical vein endothelial cells were perfused with recalcified citrated WB stimulated with monoclonal Ab KKO (50 µg/mL) in the presence of PF4 (25 µg/mL). Some samples were preincubated with C1r inhibitor [C1r(i); 5 µg/mL, 25 µg/mL, or 100 µg/mL] 15 minutes before the addition of KKO (50 µg/mL) and PF4 (25 µg/mL). Adhesion of calcein-labeled platelets was measured as total fluorescent intensity at 5-minute intervals, and the effect of C1r(i) is expressed as percentage of platelet adhesion in the presence of inhibitor compared with platelet adhesion without inhibitor (100%). *P < .05, **P < .005, ***P < .0005 (2-way analysis of variance with Dunnett’s correction); n = 4.

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