This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Purchase Article View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Johnson, R. D. Articles by Nelson, D. M. Search for Related Content PubMed PubMed Citation Articles by Johnson, R. D. Articles by Nelson, D. M.

The Expression and Activity of Prostaglandin H Synthase-2 Is Enhanced in Trophoblast from Women with Preeclampsia¹

Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, Missouri 63110

Address all correspondence and requests for reprints to: D. Michael Nelson, M.D., Ph.D., Department of Obstetrics and Gynecology, 4911 Barnes Hospital Plaza, St. Louis, Missouri 63110-1094. NELSON DM{at}kids.wustl.edu

Preeclampsia is associated with altered biosynthesis of vasoactive prostanoids in placental villi. The two isozymes of prostaglandin H synthase (PGHS) are essential for prostanoid synthesis. We tested the hypothesis that PGHS-2 expression is elevated in trophoblast from preeclamptic women, compared with trophoblast from healthy women. Using immunofluorescent staining, we demonstrated a higher PGHS-2 expression in villi from preeclampsia, compared with normal pregnancy. Cytotrophoblasts cultured from placentas of preeclamptic women expressed higher levels of PGHS-2 compared with cytotrophoblasts from normal placentas. This enhanced expression of PGHS-2 correlated with increased media levels of both thromboxane and prostaglandin E₂, two products of PGHS activity. The increased prostanoid production by trophoblast from preeclamptic women was markedly reduced by NS-398, a specific inhibitor of PGHS-2. We conclude that both expression and activity of PGHS-2 are enhanced in trophoblasts from preeclamptic women compared with trophoblast from normal pregnancies. The increased production of prostanoids may contribute to the clinical syndrome of preeclampsia. Our data suggest that a selective inhibitor of PGHS-2 might provide a therapeutic alternative to prophylactic low-dose aspirin in modifying the prostanoid profile in preeclampsia.

This article has been cited by other articles:

				A. Tesse, F. Meziani, E. David, N. Carusio, H. Kremer, F. Schneider, and R. Andriantsitohaina Microparticles from preeclamptic women induce vascular hyporeactivity in vessels from pregnant mice through an overproduction of NO Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H520 - H525. [Abstract] [Full Text] [PDF]

				F. Meziani, A. Tesse, E. David, M. C. Martinez, R. Wangesteen, F. Schneider, and R. Andriantsitohaina Shed Membrane Particles from Preeclamptic Women Generate Vascular Wall Inflammation and Blunt Vascular Contractility Am. J. Pathol., October 1, 2006; 169(4): 1473 - 1483. [Abstract] [Full Text] [PDF]

				R. Thadhani, W. P. Mutter, M. Wolf, R. J. Levine, R. N. Taylor, V. P. Sukhatme, J. Ecker, and S. A. Karumanchi First Trimester Placental Growth Factor and Soluble Fms-Like Tyrosine Kinase 1 and Risk for Preeclampsia J. Clin. Endocrinol. Metab., February 1, 2004; 89(2): 770 - 775. [Abstract] [Full Text] [PDF]

				S. T. Davidge Prostaglandin H Synthase and Vascular Function Circ. Res., October 12, 2001; 89(8): 650 - 660. [Abstract] [Full Text] [PDF]