PMID- 10086076 OWN - NLM STAT- MEDLINE DCOM- 19990415 LR - 20170404 IS - 1354-4195 (Print) IS - 1354-4195 (Linking) VI - 3 IP - 4 DP - 1997 Dec TI - Human endometrial decidual cell-associated 11 beta-hydroxysteroid dehydrogenase expression: its potential role in implantation. PG - 259-64 AB - During pregnancy excess corticosteroid exposure can disturb the normal pattern of growth and differentiation of the primate fetus. This is normally prevented by the action of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), which converts cortisol to its biologically inactive 11-oxo form, thereby ensuring that little or no cortisol is transferred to the fetus. During implantation, extravillous trophoblasts breech uterine vessels that are embedded in a decidual cell matrix. Through this invasive process the embryo gains requisite access to the maternal blood supply, while risking exposure to high circulating glucocorticoid levels. Thus, the expression of 11 beta-HSD by the decidual cell layer may be essential in regulating cortisol exposure of the developing embryo prior to placentation. In order to investigate the potential contribution of decidual cells to glucocorticoid metabolism, we evaluated the expression of both known 11 beta-HSD isoforms, 11 beta-HSD1, whose catalytic activity is NADP(+)-dependent, and NAD(+)-dependent 11 beta-HSD2, during decidualization of monolayers of human endometrial stromal cells. The differential actions of ovarian steroids on human endometrium are simulated in this in vitro model. Thus, progestins induce the expression of several decidualization markers in the cultured stromal cells, and consistent with its priming action in vivo, estradiol augments this expression. The results of our studies established a link between in vitro decidualization and enhanced glucocorticoid metabolizing capacity. Accordingly, the catalytic activities of both 11 beta-HSD isoforms were enhanced by incubation of the precursor stromal cells with medroxyprogesterone acetate, and further enhanced by estradiol, despite a lack of response to estradiol alone. This differential response to estradiol and progestin was reflected in parallel changes in steady state levels of 11 beta-HSD1 messenger RNA. The role of glucocorticoid metabolizing activity of the decidual cell is discussed in terms of its implications in determining the exposure of the implanting embryo to biologically active glucocorticoids. FAU - Arcuri, F AU - Arcuri F AD - Institute of Pathologic Anatomy and Histology, New York University Medical Center 10016, USA. FAU - Battistini, S AU - Battistini S FAU - Hausknecht, V AU - Hausknecht V FAU - Cintorino, M AU - Cintorino M FAU - Lockwood, C J AU - Lockwood CJ FAU - Schatz, F AU - Schatz F LA - eng GR - R29 HD29540/HD/NICHD NIH HHS/United States PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Early Pregnancy JT - Early pregnancy : biology and medicine : the official journal of the Society for the Investigation of Early Pregnancy JID - 9508879 RN - 0 (Isoenzymes) RN - 4TI98Z838E (Estradiol) RN - 63231-63-0 (RNA) RN - EC 1.1.- (Hydroxysteroid Dehydrogenases) RN - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases) RN - FO4V44A3G3 (11-dehydrocorticosterone) RN - HSU1C9YRES (Medroxyprogesterone) RN - W980KJ009P (Corticosterone) SB - IM MH - 11-beta-Hydroxysteroid Dehydrogenases MH - Blotting, Northern MH - Chromatography, Thin Layer MH - Corticosterone/analogs & derivatives/analysis/metabolism MH - Decidua/*enzymology/metabolism MH - Embryo Implantation/*physiology MH - Estradiol/metabolism MH - Female MH - *Gene Expression Regulation, Developmental MH - Humans MH - Hydroxysteroid Dehydrogenases/*genetics/physiology MH - Isoenzymes MH - Medroxyprogesterone/metabolism MH - Pregnancy MH - RNA/chemistry MH - Stromal Cells/enzymology EDAT- 1999/03/23 00:00 MHDA- 1999/03/23 00:01 CRDT- 1999/03/23 00:00 PHST- 1999/03/23 00:00 [pubmed] PHST- 1999/03/23 00:01 [medline] PHST- 1999/03/23 00:00 [entrez] PST - ppublish SO - Early Pregnancy. 1997 Dec;3(4):259-64.