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Platelets decrease albumin permeability of pulmonary artery endothelial cell monolayers

1989; Elsevier BV; Volume: 37; Issue: 3 Linguagem: Inglês

10.1016/0026-2862(89)90044-7

1095-9319

J. M. Shepard, Dudley G. Moon, P. F. Sherman, Lisa K Weston, Peter J. Del Vecchio, Fred L. Minnear, Asrar B. Malik, John Kaplan,

Inflammatory Biomarkers in Disease Prognosis

Since platelets may modulate endothelial cell permeability, we examined the effects of platelets on 125I-albumin permeability of cultured bovine pulmonary artery endothelial cell monolayers. The experimental system consisted of endothelial cells grown to confluence on a gelatinized polycarbonate filter. We quantified the diffusive flux of 125I-albumin from luminal chamber to the abluminal chamber. Washed human platelets added to the monolayers decreased the albumin flux in a concentration-dependent manner, with a 65% decrease occurring at the highest concentration of platelets (5 × 107 platelets) added to the 700-μl luminal chamber. In contrast, neither paraformaldehyde-fixed platelets nor fresh red blood cells changed 125I-albumin permeability. Platelets had no effect on 125I-albumin permeability across the gelatinized filters without endothelial cells present. Supernatants of platelet lysates also reduced albumin flux. The effect produced by intact platelets or platelet lysate was not influenced by the presence of ketanserin (a serotonin receptor antagonist), propranolol (a β-adrenergic receptor antagonist), or aspirin (an inhibitor of cyclooxygenase). Platelets activated by thrombin did not produce an effect that was different from the effect produced by intact platelets. The activity of the supernatant of platelet lysate remained in the aqueous phase after ether extraction. The results indicate that the platelet-mediated decrease in endothelial cell permeability to 125I-albumin is the result of a hydrophilic platelet-derived factor(s) and not secondary to mechanical obstruction of endothelial “leaks” by the platelets.