Spatial and temporal changes in the expression of steroid hormone receptors in mouse model of endometriosis.
IF: 3.357
Cited by: 7


Endometriosis is recognized as a steroid hormone-dependent disorder. However, controversies exist regarding the status of the steroid hormone receptor expression in endometriotic tissues. The purpose of this study was to determine the ontogeny of cellular changes in the expression of estrogen receptors (ERα, ERβ), G protein-coupled estrogen receptor 1 (GPER1), and progesterone receptors (PRs) in endometriosis using a mouse model. We used the autologous uterine tissue transfer mouse model and studied the mRNA and protein expression of ERα, ERβ, GPER1, and PR in ectopic lesions at 2, 4, and 8 weeks of induction of endometriosis. As compared to endometrium of controls, in the ectopic endometrium, ERα is reduced while ERβ was elevated in stromal cells; however, Gper1 and PR levels are reduced in both stromal and epithelial cells in a time-specific manner. There is a high inter-animal variation in the levels of these receptors in ectopic endometrium as compared to controls; the levels also varied by almost 100-fold within the same lesion resulting in "micro-heterogeneity." The expression of all these receptors also deferred between two lesions from the same animal. In the endometriotic tissue, there is extensive inter-animal and intra-lesion heterogeneity in the expression of ERα, ERβ, GPER1, and PR. These changes are not due to the influence of the peritoneal environment but appear to be tissue intrinsic. We propose that the variable outcomes in hormonal therapy for endometriosis could be possibly due to heterogeneity in the expression of steroid hormone receptors in the ectopic endometrium.


Estrogen receptor
Progesterone receptor
Steroid hormone receptors

MeSH terms

Disease Models, Animal
Estrogen Receptor alpha
Estrogen Receptor beta
Gene Expression Regulation, Developmental
Gonadal Steroid Hormones
Receptors, Estrogen
Receptors, G-Protein-Coupled
Receptors, Progesterone


Mishra, Anuradha
Galvankar, Mosami
Singh, Neha
Modi, Deepak