Figure 5.
Anti-β3 PSI domain monoclonal antibodies inhibited platelet aggregation in vitro. Murine or human PRP or gel-filtered platelet (2.5 × 108/mL) was incubated with anti-PSI mAb. Platelet aggregation was induced by agonist and monitored using aggregometer. (A) Anti-PSI mAbs (40 μg/mL) inhibited ADP (20 μM)-induced aggregation of murine PRP. (B) Anti-PSI mAbs also inhibited ADP (5 μM)-induced aggregation of human PRP. (C) Anti-PSI mAbs inhibited TRAP (250 μM) and collagen (10 μg/mL)-induced aggregation of human PRP (representative of n = 3-4). (D) Anti-PSI mAbs inhibited thrombin (1 U/mL), TRAP (250 μM), and collagen (10 μg/mL)–induced human gel-filtered platelet aggregation (representative of n = 3-4). Mean ± SEM; *P < .05, **P < .01, ***P < .001.

Anti-β3 PSI domain monoclonal antibodies inhibited platelet aggregation in vitro. Murine or human PRP or gel-filtered platelet (2.5 × 108/mL) was incubated with anti-PSI mAb. Platelet aggregation was induced by agonist and monitored using aggregometer. (A) Anti-PSI mAbs (40 μg/mL) inhibited ADP (20 μM)-induced aggregation of murine PRP. (B) Anti-PSI mAbs also inhibited ADP (5 μM)-induced aggregation of human PRP. (C) Anti-PSI mAbs inhibited TRAP (250 μM) and collagen (10 μg/mL)-induced aggregation of human PRP (representative of n = 3-4). (D) Anti-PSI mAbs inhibited thrombin (1 U/mL), TRAP (250 μM), and collagen (10 μg/mL)–induced human gel-filtered platelet aggregation (representative of n = 3-4). Mean ± SEM; *P < .05, **P < .01, ***P < .001.

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