Figure 7
Figure 7. Effects of rabbit polyclonal antibody against PSR on sickle erythrocyte adhesion to human lung microendothelial cells. Following incubation of endothelial cells for 6 hours in the presence or absence of IL-1α (10 ng/mL), cell monolayers were pretreated with rabbit polyclonal antibody against PSR (at 20 μg/mL) for 30 minutes. The monolayers were then tested for their adhesive potential using red cells from patients with sickle cell disease (HbSS genotype). Adhesion assays were performed using red cells at 10% hematocrit in the absence of plasma and plasma-associated soluble adhesion ligands. Panels A and B represent adhesion of HbSS erythrocytes with low PS positivity (1.0% ± 0.8% positivity) and high PS positivity (7.0% ± 2.8% positivity), respectively. Results presented are the mean (± SD) from 4 (A) or 5 (B) experiments. Adhesion of sickle red cells to test endothelium was presented as fold change compared with adhesion of control red cells to unactivated endothelial cells. *P = .05 compared with the IL-1α control.

Effects of rabbit polyclonal antibody against PSR on sickle erythrocyte adhesion to human lung microendothelial cells. Following incubation of endothelial cells for 6 hours in the presence or absence of IL-1α (10 ng/mL), cell monolayers were pretreated with rabbit polyclonal antibody against PSR (at 20 μg/mL) for 30 minutes. The monolayers were then tested for their adhesive potential using red cells from patients with sickle cell disease (HbSS genotype). Adhesion assays were performed using red cells at 10% hematocrit in the absence of plasma and plasma-associated soluble adhesion ligands. Panels A and B represent adhesion of HbSS erythrocytes with low PS positivity (1.0% ± 0.8% positivity) and high PS positivity (7.0% ± 2.8% positivity), respectively. Results presented are the mean (± SD) from 4 (A) or 5 (B) experiments. Adhesion of sickle red cells to test endothelium was presented as fold change compared with adhesion of control red cells to unactivated endothelial cells. *P = .05 compared with the IL-1α control.

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