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Endometrial expression of estrogen receptor β and its splice variants in patients with and without endometriosis.

18:13 EDT 24th April 2014 | BioPortfolio

Summary of "Endometrial expression of estrogen receptor β and its splice variants in patients with and without endometriosis."


BACKGROUND:
The role of estrogen receptor beta (ERβ) in pathogenesis of endometriosis remains to be elucidated. In this study, we have examined the expression of the four main ERβ transcript isoforms in human endometrial tissue in women with or without endometriosis.
METHODS:
Total RNA was isolated from native endometrial tissue and transcript levels of ERα, β1, β2, β4, β5 were analyzed by means of RT-PCR. We compared the results with regard to menstrual cycle phase as well as to presence or absence of endometriosis. We prospectively harvested the endometrium of ten women without endometriosis (five for each cycle phase) and eight patients with endometriosis (five in the proliferative phase, three in the secretory phase).
RESULTS:
ERα, β1, β2, and β5 transcripts were detected in both cycle phases. During the proliferative phase, healthy women had a significantly higher ERα/ERβ1-ratio than patients with endometriosis. Irrespective of the cycle phase, ERα-mRNA level was significantly higher than transcript levels of ERβ isoforms.
CONCLUSIONS:
ERα, β1, β2, and β5 are expressed in human endometrium. The individual receptors differed in terms of expression strength but there was no relevant change during the cycle. The decreased ERα/ERβ1-ratio in proliferative endometrium of endometriosis patients suggest that ERβ1 might be involved in the pathogenesis of endometriosis. Further studies should be undertaken to substantiate the role of ERβ in endometrial pathology.

Affiliation

Department of Obstetrics and Gynecology, University of Regensburg, Landshuterstr. 53, 93053, Regensburg, Germany, ingolf.juhasz-boess@klinik.uni-r.de.

Journal Details

This article was published in the following journal.

Name: Archives of gynecology and obstetrics
ISSN: 1432-0711
Pages:

Links

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