Endotoxin-induced secretion of an active plasminogen activator inhibitor from bovine pulmonary arterial and aortic endothelial cells.
Treatment of bovine pulmonary arterial and aortic endothelial cells for 24 h with 10-20 ng/ml endotoxin appeared to suppress urokinase secretion by over 90%. Immunodepletion of urokinase from conditioned medium revealed high levels of a fully active plasminogen activator inhibitor (PAI). In contrast, medium from aortic cells not treated with endotoxin expressed low levels of a latent PAI. The endotoxin-induced PAI from both cell types was not immunoprecipitated by incubation with IgG directed against the endothelial-type inhibitor, PAI-1, or antiserum directed against the placental-type inhibitor, PAI-2. Endotoxin-induced PAI was inactivated by 0.2-1.0 M of 2-mercaptoethanol, but unaffected by treatment with up to 500 microM of chloramine-T. We conclude that the exposure of bovine endothelial cells to endotoxin causes the secretion of a fully active PAI with properties different from those reported for PAI-1.
D000818:Animals; D001011:Aorta / Q000166:cytology; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000201:enzymology*; D004731:Endotoxins / Q000494:pharmacology*; D006023:Glycoproteins / Q000276:immunology / Q000378:metabolism*; D007158:Immunologic Techniques; D010084:Oxidation-Reduction; D010960:Plasminogen Activators / Q000037:antagonists & inhibitors*; D015849:Plasminogen Inactivators; D011651:Pulmonary Artery / Q000166:cytology; D012636:Secretory Rate / Q000187:drug effects
D004731:Endotoxins; D006023:Glycoproteins; D015849:Plasminogen Inactivators; D010960:Plasminogen Activators