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The regulation of plasminogen activators and plasminogen activator inhibitor type 1 in endothelial cells by sex hormones



The regulation of plasminogen activators and plasminogen activator inhibitor type 1 in endothelial cells by sex hormones



American Journal of Obstetrics & Gynecology 173(3 PART 1): 801-808



OBJECTIVE: The purpose of this study was to assess the effect of 17-beta-estradiol, progesterone, and testosterone on secretion of plasminogen activators and plasminogen activator inhibitor type 1 by cultured endothelial cells. STUDY DESIGN: Bovine aortic endothelial cells were cultured in medium that contained 17-beta-estradiol, progesterone, or testosterone at various concentrations (10-13 to 10-6 mol/L). Plasminogen activator activity in culture medium in the presence of cells was assayed after a 36-hour incubation using chromogenic substrate and iodine 125-labeled fibrin plate assays. Plasminogen activator inhibitor type 1 antigen was detected in conditioned media of bovine aortic endothelial cells by Western blotting analysis. RESULTS: All three steroid hormones exhibited biphasic dose-response effects, characterized by stimulation of plasminogen activator secretion at lower concentrations and inhibition of plasminogen activator secretion at higher concentrations. A significant stimulatory effect on plasminogen activator secretion (74% over control) was observed at a 17-beta-estradiol concentration of 10-12 mol/L (p lt 0.03). At higher concentrations of 17-beta-estradiol, progesterone, and testosterone, inhibition of plasminogen activator secretion was observed (p lt 0.05). Decreased levels of plasminogen activator inhibitor type 1 antigen were detected in supernatants treated with either 17-beta-estradiol or progesterone at a concentration of 10-12 mol/L and were maximal at 10-7 mol/L 17-beta-estradiol, progesterone, and a concentration of CONCLUSION: The secretion of plasminogen activators and plasminogen activator inhibitor type 1 is regulated in a biphasic dose-dependent manner by sex hormones in bovine aortic endothelial cells.

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Accession: 009613968

Download citation: RISBibTeXText

PMID: 7573247

DOI: 10.1016/0002-9378(95)90344-5



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