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Role of Estrogen Receptor-β in Endometriosis

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Date 2012 Jan 25
PMID 22271293
Citations 125
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Abstract

Endometriosis is an estrogen-dependent disease. The biologically active estrogen, estradiol, aggravates the pathological processes (e.g., inflammation and growth) and the symptoms (e.g., pain) associated with endometriosis. Abundant quantities of estradiol are available for endometriotic tissue via several mechanisms including local aromatase expression. The question remains, then, what mediates estradiol action. Because estrogen receptor (ER)β levels in endometriosis are >100 times higher than those in endometrial tissue, this review focuses on this nuclear receptor. Deficient methylation of the ERβ promoter results in pathological overexpression of ERβ in endometriotic stromal cells. High levels of ERβ suppress ERα expression. A severely high ERβ-to-ERα ratio in endometriotic stromal cells is associated with suppressed progesterone receptor and increased cyclo-oxygenase-2 levels contributing to progesterone resistance and inflammation. ERβ-selective estradiol antagonists may serve as novel therapeutics of endometriosis in the future.

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References
1.
Vercellini P, Trespidi L, De Giorgi O, Cortesi I, Parazzini F, Crosignani P . Endometriosis and pelvic pain: relation to disease stage and localization. Fertil Steril. 1996; 65(2):299-304. View

2.
Petz L, Ziegler Y, Schultz J, Nardulli A . Fos and Jun inhibit estrogen-induced transcription of the human progesterone receptor gene through an activator protein-1 site. Mol Endocrinol. 2003; 18(3):521-32. DOI: 10.1210/me.2003-0105. View

3.
Savouret J, Bailly A, Misrahi M, Rauch C, Redeuilh G, Chauchereau A . Characterization of the hormone responsive element involved in the regulation of the progesterone receptor gene. EMBO J. 1991; 10(7):1875-83. PMC: 452862. DOI: 10.1002/j.1460-2075.1991.tb07713.x. View

4.
Montano M, Kraus W, Katzenellenbogen B . Identification of a novel transferable cis element in the promoter of an estrogen-responsive gene that modulates sensitivity to hormone and antihormone. Mol Endocrinol. 1997; 11(3):330-41. DOI: 10.1210/mend.11.3.9899. View

5.
Vercellini P, Cortesi I, Crosignani P . Progestins for symptomatic endometriosis: a critical analysis of the evidence. Fertil Steril. 1997; 68(3):393-401. DOI: 10.1016/s0015-0282(97)00193-3. View