| Role of Estrogen Receptor-β in Endometriosis. | |
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MedLine Citation:
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PMID: 22271293 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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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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Authors:
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Serdar E Bulun; Diana Monsavais; Mary Ellen Pavone; Matthew Dyson; Qing Xue; Erkut Attar; Hideki Tokunaga; Emily J Su |
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Publication Detail:
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Type: Journal Article Date: 2012-01-23 |
Journal Detail:
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Title: Seminars in reproductive medicine Volume: 30 ISSN: 1526-4564 ISO Abbreviation: Semin. Reprod. Med. Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2012-01-24 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100909394 Medline TA: Semin Reprod Med Country: United States |
Other Details:
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Languages: eng Pagination: 39-45 Citation Subset: IM |
Copyright Information:
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Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA. |
Affiliation:
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Division of Reproductive Biology Research, Department Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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