Figure 3.
Figure 3. PECAM-1–deficient platelets display normal static platelet adhesion on fibrinogen and bovine VWF matrices. Anticoagulated whole blood from PECAM-1+/+ and PECAM-1–/– mice was labeled with DiOC6 (50 μg/mL) and washed platelets were isolated. Labeled platelets (1 × 109/mL) were then allowed to adhere to bovine serum albumin (BSA)–coated (100 μg/mL) coverslips, collagen-coated (2.5 mg/mL) coverslips, fibrinogen-coated (100 μg/mL) coverslips, or bovine VWF–coated (20 μg/mL) coverslips in the presence of botrocetin (1 μg/mL) for 0 to 60 minutes at 37°C. Adherent platelets were fixed at different time points and visualized using fluorescence microscopy. Quantitation of adherent PECAM-1+/+ and PECAM-1–/– platelets was determined by analysis of images acquired using a × 100 objective. These data represent the mean ± SEM from 3 independent experiments. *P < .05 (n = 3).

PECAM-1–deficient platelets display normal static platelet adhesion on fibrinogen and bovine VWF matrices. Anticoagulated whole blood from PECAM-1+/+ and PECAM-1–/– mice was labeled with DiOC6 (50 μg/mL) and washed platelets were isolated. Labeled platelets (1 × 109/mL) were then allowed to adhere to bovine serum albumin (BSA)–coated (100 μg/mL) coverslips, collagen-coated (2.5 mg/mL) coverslips, fibrinogen-coated (100 μg/mL) coverslips, or bovine VWF–coated (20 μg/mL) coverslips in the presence of botrocetin (1 μg/mL) for 0 to 60 minutes at 37°C. Adherent platelets were fixed at different time points and visualized using fluorescence microscopy. Quantitation of adherent PECAM-1+/+ and PECAM-1–/– platelets was determined by analysis of images acquired using a × 100 objective. These data represent the mean ± SEM from 3 independent experiments. *P < .05 (n = 3).

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