Estrogen receptor β agonist inhibits proliferation of endometrial stromal cells in an estrogen-receptor independent manner

In: Archives of Biological Sciences · 2014 · vol. 66(2) , pp. 735–741 · doi:10.2298/abs1402735x · W2057255926
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Diarylpropionitrile, an ERβ agonist, inhibited human endometrial stromal cell proliferation independently of ERβ, despite ERβ expression being absent in endometrial stromal cells.

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This study investigated whether an estrogen receptor beta (ERβ) agonist, diarylpropionitrile (DPN), affects proliferation of human endometrial stromal cells and whether functional ERβ is present in eutopic and ectopic endometrium. The authors assessed ERβ mRNA and protein expression in both eutopic and ectopic endometrium and used a luciferase reporter assay to test for functional ERβ in human endometrial stromal cells. DPN significantly inhibited endometrial stromal cell proliferation at 10 μM by 25% but not at 10 nM, and although ERβ mRNA was detectable in both eutopic and ectopic endometrium, ERβ protein expression and functional ERβ activity were absent in stroma and epithelium. This paper is centrally about endometriosis — it tests whether ERβ agonist–induced effects on endometrial stromal proliferation may be ERβ-independent and discusses implications for regression of ectopic endometrial implants.

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Abstract

The finding that estrogen receptor ER? agonists induce regression of ectopic endometrial implants in a rodent model has rekindled interest in the role of ER? in the growth and maintenance of human endometriosis. We hypothesize that the ER? agonist may have a direct effect on the human endometrium. We examined the mRNA and protein expression of ER? in both eutopic and ectopic endometrium and performed a luciferase reporter assay for the presence of functional ER? in human endometrial stromal cells. Diarylpropionitrile (DPN - a ER? specific agonist) significantly inhibited endometrial stromal cell proliferation at 10 M by 25% but not at 10 nM. ER? mRNA is present in both eutopic and ectopic endometrium; however, protein expression is absent in both stroma and epithelium. Our search for functional ER? similarly showed an absence in endometrial stromal cells. These results suggest that the regression of endometriosis might be ER?-independent.
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Archives of Biological Sciences 2014 Volume 66, Issue 2, Pages: 735-741 Estrogen receptor β agonist inhibits proliferation of endometrial stromal cells in an estrogen-receptor independent manner Xia Qiong (Wuhan Puai Hospital, Department of Obstetrics, Gynecology, Wuhan, China) The finding that estrogen receptor ERβ agonists induce regression of ectopic endometrial implants in a rodent model has rekindled interest in the role of ERβ in the growth and maintenance of human endometriosis. We hypothesize that the ERβ agonist may have a direct effect on the human endometrium. We examined the mRNA and protein expression of ERβ in both eutopic and ectopic endometrium and performed a luciferase reporter assay for the presence of functional ERβ in human endometrial stromal cells. Diarylpropionitrile (DPN - a ERβ specific agonist) significantly inhibited endometrial stromal cell proliferation at 10 M by 25% but not at 10 nM. ERβ mRNA is present in both eutopic and ectopic endometrium; however, protein expression is absent in both stroma and epithelium. Our search for functional ERβ similarly showed an absence in endometrial stromal cells. These results suggest that the regression of endometriosis might be ERβ-independent. Keywords: endometrium, neoplasm, pathology, estrogen, receptor https://doi.org/10.2298/ABS1402735X Full text ( 628 KB) Zhao Dong (Tongji University School of Medicine, Shanghai First Maternity and Infant Hospital, Department of Obstetrics, Gynecology, Shanghai, China) Wang Juan (Department of Obstetrics, Gynecology, Wuhan Puai Hospital, Wuhan, China)

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endometriosis

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