Figure 8.
Figure 8. Arrest of flow platelets incubated with or without blocking anti-CD36, anti-CD47, or the 2 mAbs successively on TNF-α–treated endothelial cells. EA endothelial cells were grown onto permanox Lab-Tek 1 chamber slides and stimulated with 25 ng/mL rh TNF-α for 18 hours. Platelets were first labeled with calceine in PRP and then were incubated or not incubated with 40 μg/mL anti-CD36 mAb FA6.152 or anti-CD47 mAb B6H12 for 10 minutes at 37°C or with the 2 mAbs successively. Whole blood was reconstituted and perfused through the chamber at 37°C and at a shear rate of 100 seconds–1 for 3 minutes. Platelet adhesion, expressed as percentage of surface covered with platelets, is the average ± SEM of 10 random fields per coverslip. ***P < .001. This experiment is representative of 3 experiments performed using blood from different donors.

Arrest of flow platelets incubated with or without blocking anti-CD36, anti-CD47, or the 2 mAbs successively on TNF-α–treated endothelial cells. EA endothelial cells were grown onto permanox Lab-Tek 1 chamber slides and stimulated with 25 ng/mL rh TNF-α for 18 hours. Platelets were first labeled with calceine in PRP and then were incubated or not incubated with 40 μg/mL anti-CD36 mAb FA6.152 or anti-CD47 mAb B6H12 for 10 minutes at 37°C or with the 2 mAbs successively. Whole blood was reconstituted and perfused through the chamber at 37°C and at a shear rate of 100 seconds1 for 3 minutes. Platelet adhesion, expressed as percentage of surface covered with platelets, is the average ± SEM of 10 random fields per coverslip. ***P < .001. This experiment is representative of 3 experiments performed using blood from different donors.

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