Results
| PMID | 22271293 |
| Gene Name | ESR2 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Other associated phenotypes |
Endometriosis |
|
Semin Reprod Med. 2012 Jan;30(1):39-45. doi: 10.1055/s-0031-1299596. Epub 2012 Bulun, Serdar E| Monsavais, Diana| Pavone, Mary Ellen| Dyson, Matthew| Xue, Qing| Attar, Erkut| Tokunaga, Hideki| Su, Emily J Division of Reproductive Biology Research, Department Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA. s-bulun@northwestern.edu 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)beta levels in endometriosis are >100 times higher than those in endometrial tissue, this review focuses on this nuclear receptor. Deficient methylation of the ERbeta promoter results in pathological overexpression of ERbeta in endometriotic stromal cells. High levels of ERbeta suppress ERalpha expression. A severely high ERbeta-to-ERalpha ratio in endometriotic stromal cells is associated with suppressed progesterone receptor and increased cyclo-oxygenase-2 levels contributing to progesterone resistance and inflammation. ERbeta-selective estradiol antagonists may serve as novel therapeutics of endometriosis in the future. Mesh Terms: 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 |
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