Role of estrogen receptor-β in endometriosis

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) levels in endometriosis are >100 times higher than those in endometrial tissue, this review focuses on this nuclear receptor. Deficient methylation of the ER promoter results in pathological overexpression of ER in endometriotic stromal cells. High levels of ER suppress ER expression. A severely high ER-βto-ER ratio in endometriotic stromal cells is associated with suppressed progesterone receptor and increased cyclo-oxygenase-2 levels contributing to progesterone resistance and inflammation. ER-βselective estradiol antagonists may serve as novel therapeutics of endometriosis in the future. © 2011 Kabeerdoss et al; licensee BioMed Central Ltd.