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Updated: Aug 13, 2026

Prostaglandin Extraction and Analysis in Caenorhabditis elegans
Published on: June 25, 2013
Estrogen decreases prostaglandin H synthase products from endothelial cells
K G Stewart1, Y Zhang, S T Davidge
1Department of Obstetrics/Gynecology, University of Alberta, Edmonton, Canada.
Objective:
Because we showed recently that estrogen replacement prevents prostaglandin H synthase (PGHS)-dependent vasoconstriction in rats, the aim of this study was to determine how estradiol affects production of PGHS-dependent eicosanoids.
Methods:
Cultured bovine coronary microvascular endothelial cells were exposed to physiologic levels of 17 beta-estradiol (0.01 nM [about 2.7 pg/mL], 0.1 nM [about 27 pg/mL], or 1.0 nM [about 270 pg/mL]) for 4, 8, or 24 hours. Thromboxane (TXA2), prostacyclin (PGI2), and nitric oxide (NO) were measured as their stable metabolites, thromboxane B2 (TXB2), 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha), and nitrite (NO2), respectively.
Results:
Estradiol had no effect on nitrite production. However, exposure to 0.1 nM and 1.0 nM estradiol for 24 hours reduced TXB2 production to 67 +/- 16% and 69 +/- 12% of control, respectively. Furthermore, 0.1 nM and 1.0 nM estradiol also reduced production of 6-keto PGF1 alpha to 35 +/- 19% and 17 +/- 11% of control, respectively. Prostaglandin H synthase expression was not altered by estradiol. However, the estrogen receptor inhibitor, tamoxifen, reversed the inhibitory effect of estradiol.
Conclusion:
Estradiol acts through a receptor-dependent process to decrease PGHS-dependent products, thus further elucidating this novel effect of estradiol on the vascular system.
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