Document Detail


Role of estrogen receptor-β in endometriosis.
MedLine Citation:
PMID:  22271293     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2012-01-23
Journal Detail:
Title:  Seminars in reproductive medicine     Volume:  30     ISSN:  1526-4564     ISO Abbreviation:  Semin. Reprod. Med.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-24     Completed Date:  2012-05-14     Revised Date:  2014-05-29    
Medline Journal Info:
Nlm Unique ID:  100909394     Medline TA:  Semin Reprod Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  39-45     Citation Subset:  IM    
Copyright Information:
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cyclooxygenase 2 / genetics,  metabolism
Endometriosis / drug therapy,  enzymology,  metabolism*
Endometrium / drug effects,  enzymology,  metabolism*
Epigenesis, Genetic / drug effects
Estrogen Antagonists / pharmacology,  therapeutic use
Estrogen Receptor alpha / genetics,  metabolism
Estrogen Receptor beta / agonists,  antagonists & inhibitors,  genetics,  metabolism*
Estrogens / chemistry,  metabolism*
Female
Gene Expression Regulation / drug effects
Humans
Molecular Targeted Therapy
Promoter Regions, Genetic / drug effects
Receptors, Progesterone / genetics,  metabolism
Signal Transduction* / drug effects
Steroidogenic Factor 1 / genetics,  metabolism
Stromal Cells / drug effects,  enzymology,  metabolism
Grant Support
ID/Acronym/Agency:
K12 HD050121/HD/NICHD NIH HHS; R37-HD37691/HD/NICHD NIH HHS; T32 DK007169/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Estrogen Antagonists; 0/Estrogen Receptor alpha; 0/Estrogen Receptor beta; 0/Estrogens; 0/NR5A1 protein, human; 0/Receptors, Progesterone; 0/Steroidogenic Factor 1; 0/estrogen receptor alpha, human; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/PTGS2 protein, human
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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