Semin Reprod Med 2012; 30(01): 39-45
DOI: 10.1055/s-0031-1299596
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Role of Estrogen Receptor-β in Endometriosis

Serdar E. Bulun
1   Division of Reproductive Biology Research, Department Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois
,
Diana Monsavais
1   Division of Reproductive Biology Research, Department Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois
,
Mary Ellen Pavone
1   Division of Reproductive Biology Research, Department Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois
,
Matthew Dyson
1   Division of Reproductive Biology Research, Department Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois
,
Qing Xue
2   Department of Obstetrics and Gynecology, First Hospital of Peking University, Beijing, P.R. China
,
Erkut Attar
3   Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Istanbul University Capa School of Medicine, Istanbul, Turkiye
,
Hideki Tokunaga
4   Department of Obstetrics and Gynecology, Tohoku University School of Medicine, Sendai, Japan
,
Emily J. Su
1   Division of Reproductive Biology Research, Department Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois
› Author Affiliations
Further Information

Publication History

Publication Date:
23 January 2012 (online)

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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