Figure 7.
Figure 7. Interaction of IAC-1 to platelets deposited on collagen under flow. (A-B) Anticoagulated whole human blood supplemented with 10 μg/mL IAC-1-FITC was perfused over a collagen-coated surface at a wall shear rate of 1000 s-1. (A) Platelet adhesion was determined as the percent surface coverage in the presence or absence of IAC-1-FITC. Error bars indicate the SEMs of at least 3 independent experiments. (B) Confocal microscopy analysis of adhered platelet aggregates after 4 minutes of perfusion showed that the signal of IAC-1-FITC (green) colocalized with platelets as detected by actin staining with Texas-Red phalloidin (red). (C) Postperfusion binding of FITC-labeled MOPC-21 (10 μg/mL), IAC-1 (10 μg/mL), or Gi9 (5 μg/mL) to platelets in the presence or absence of 10% ACD and 10 μM PGE1.

Interaction of IAC-1 to platelets deposited on collagen under flow. (A-B) Anticoagulated whole human blood supplemented with 10 μg/mL IAC-1-FITC was perfused over a collagen-coated surface at a wall shear rate of 1000 s-1. (A) Platelet adhesion was determined as the percent surface coverage in the presence or absence of IAC-1-FITC. Error bars indicate the SEMs of at least 3 independent experiments. (B) Confocal microscopy analysis of adhered platelet aggregates after 4 minutes of perfusion showed that the signal of IAC-1-FITC (green) colocalized with platelets as detected by actin staining with Texas-Red phalloidin (red). (C) Postperfusion binding of FITC-labeled MOPC-21 (10 μg/mL), IAC-1 (10 μg/mL), or Gi9 (5 μg/mL) to platelets in the presence or absence of 10% ACD and 10 μM PGE1.

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