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Regulation of Membrane-Associated Prostaglandin E₂ Synthase 1 in Pregnant Sheep Intrauterine Tissues by Glucocorticoid and Estradiol

Department of Obstetrics and Gynecology (Q.Z., J.C.R., W.X.W.), Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157; The University of Oklahoma Health Sciences Center (V.C., K.C., R.F.W.), Oklahoma City, Oklahoma 73104; Department of Obstretrics/Gynecology (N.U.), Kitasato University, School of Medicine, Kanagawa 228-8555, Japan; and Department of Obstetrics and Gynecology (D.H.), The Queen Mother’s Hospital, Yorkhill, Glasgow G3 8SJ, Scotland, United Kingdom

Address all correspondence and requests for reprints to: Dr. Wen Xuan Wu, Department of Obstetrics and Gynecology, Wake Forest University Baptist Medical Center, Winston Salem, North Carolina 27157. Email: wenwu@wfubmc.edu.

This study was designed to determine the regulatory effect of glucocorticoid and estradiol on expression of ovine intrauterine membrane-associated prostaglandin E₂ synthase 1 (mPTGES1) in late gestation and at labor. For gestational and labor groups, 16 pregnant ewes from 95–147 d gestational age (dGA) and four pregnant ewes at spontaneous term labor were used. The fetal glucocorticoid group, 14 pregnant ewes at 123–125 dGA with fetuses, was divided into the following groups: after sham adrenalectomy (n = 5), adrenalectomy (n = 4), and adrenalectomy with fetal cortisol replacement to late gestation levels (n = 5). For the maternal glucocorticoid group, nine pregnant ewes were treated with saline (n = 4) and three courses of maternal dexamethasone (n = 5). For the estradiol group, 10 pregnant ewes at 119–121 dGA were treated with sesame oil (n = 5) or estradiol (n = 5) to produce labor levels of estradiol in maternal plasma. Endometrial, myometrial, and placental mRNA and proteins were analyzed by Northern and Western blot and immunocytochemistry for mPTGES1. Data were analyzed by Student’s t test and ANOVA. There was a significant increase of placental mPTGES1 in late gestation. Glucocorticoids, given to the mother or fetus, significantly stimulated mPTGES1 in placenta. mPTGES1 was elevated only in the endometrium during spontaneous term labor and after estradiol treatment. The mPTGES1 was localized in the myometrial smooth muscle cells, endometrial stromal cells, and placental trophoblast cells. Our study suggested that increased expression of placental mPTGES1 throughout late gestation might result from the increased fetal and maternal circulating glucocorticoids, whereas elevated maternal plasma estradiol concentration might be responsible for the induced mPTGES1 expression in the endometrium during labor.

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