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Wild-Type Estrogen Receptor (ERß1) and the Splice Variant (ERßcx/ß2) Are Both Expressed within the Human Endometrium throughout the Normal Menstrual Cycle

Obstetrics and Gynecology Section, Department of Reproductive and Developmental Sciences, University of Edinburgh (H.O.D.C., T.A.H.), and Medical Research Council Human Reproductive Sciences Unit, Center for Reproductive Biology (R.W.K., G.S.S., P.T.K.S.), Edinburgh, United Kingdom EH16 4SB; and School of Biological and Molecular Sciences, Oxford Brookes University (L.R.E., N.P.G.), Headington, Oxford, United Kingdom OX3 0PB

Address all correspondence and requests for reprints to: Prof. Hilary Critchley, Obstetrics and Gynecology Section, Center for Reproductive Biology, University of Edinburgh Medical School, Little France Cresent Edinburgh, United Kingdom EH16 4SB. E-mail: hilary.critchley{at}ed.ac.uk.

Abstract

Estrogen action is mediated via two subtypes of the estrogen receptor (ER), usually referred to as ER and ERß. We have previously compared the spatial and temporal expressions of ER and ERß proteins in human endometrium and reported that endothelial cells exclusively express ERß. In the present study we have extended our investigations to compare the pattern of expression of wild-type (ERß1) and a newly identified ERß variant isoform (ERßcx/ß2) that lacks the ability to bind steroids.

mRNAs encoding both ERß1 and ERßcx/ß2 receptors were identified in human endometrial extracts by RT-PCR. Quantitative TaqMan R-TPCR demonstrated that levels of total mRNAs were increased significantly premenstrually as circulating progesterone levels declined. ERß1 and ERßcx/ß2 proteins were identified within multiple cell types within the endometrium using isotype-specific monoclonal antibodies; immunoexpression of ERßcx/ß2 appeared less intense than that of ERß1 in endometrial glandular epithelium and endothelial cells. Immunoexpression of ERß1 appeared unchanged throughout the menstrual cycle. In contrast, levels of ERßcx/ß2-specific immunoreactivity were specifically reduced in gland cells within the functional layer, but not in those of the basal layer, in the midsecretory phase. It is possible that coexpression of ERßcx/ß2 in cells containing ERß1 and/or ER may modulate the effects of estrogens on the endometrium.

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