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Expression and Localization of Endothelial Monocyte-Activating Polypeptide II in the Human Endometrium across the Menstrual Cycle: Regulation of Expression by Prostaglandin E₂

Medical Research Council Human Reproductive Sciences Unit (S.B., S.C.B., H.N.J.) and Department of Obstetrics and Gynaecology (H.O.D.C.), University of Edinburgh, Centre for Reproductive Biology, Edinburgh EH3 9ET, United Kingdom

Address all correspondence and requests for reprints to: Dr. H. N. Jabbour, Medical Research Council Human Reproductive Sciences Unit, Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3 9ET, United Kingdom. E-mail: . h.jabbour{at}hrsu.mrc.ac.uk

Abstract

A role for prostaglandins (PGs) in the regulation of endometrial functions, such as menstruation, has been established, although the mechanisms by which this is achieved are not fully elucidated. In the present study, cDNA array analysis has identified endothelial monocyte-activating polypeptide II (EMAP II) as a PGE₂-regulated gene in endometrial epithelial cells. Incubation of endometrial epithelial cells with 100 nM PGE₂ for 4 and 24 h resulted in a 2.3- and 16-fold decrease in EMAP II expression, respectively. In endometrial tissue collected across the menstrual cycle, a significant increase in EMAP II mRNA was observed during the late secretory phase, compared with the proliferative and early-midsecretory phases. The temporal pattern of EMAP II expression was confirmed further by Western blotting; EMAP II protein expression was detected as a 43-kDa band. In situ hybridization and immunohistochemistry localized EMAP II mRNA and protein expression in glandular epithelial, endothelial, and stromal cells in the functionalis and basalis layers of the endometrium. Finally, the role of PGE₂ in the regulation of EMAP II expression in the endometrium was assessed. Incubation of fresh endometrial tissue (n = 5) with 3 µg/ml indomethacin resulted in an increase in EMAP II protein expression, compared with control untreated tissue. However, cotreatment of the cells with 100 nM PGE₂ resulted in a significant decrease in EMAP II protein expression, compared with tissue incubated with indomethacin alone (P < 0.05). These data confirm temporal variation in EMAP II expression in the human endometrium across the menstrual cycle and localize expression to glandular epithelial, endothelial, and stromal cells. Moreover, EMAP II expression is negatively regulated by PGE₂.

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