| First Author | Han SJ | Year | 2015 |
| Journal | Cell | Volume | 163 |
| Issue | 4 | Pages | 960-74 |
| PubMed ID | 26544941 | Mgi Jnum | J:228035 |
| Mgi Id | MGI:5704281 | Doi | 10.1016/j.cell.2015.10.034 |
| Citation | Han SJ, et al. (2015) Estrogen Receptor beta Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis. Cell 163(4):960-74 |
| abstractText | Alterations in estrogen-mediated cellular signaling play an essential role in the pathogenesis of endometriosis. In addition to higher estrogen receptor (ER) beta levels, enhanced ERbeta activity was detected in endometriotic tissues, and the inhibition of enhanced ERbeta activity by an ERbeta-selective antagonist suppressed mouse ectopic lesion growth. Notably, gain of ERbeta function stimulated the progression of endometriosis. As a mechanism to evade endogenous immune surveillance for cell survival, ERbeta interacts with cellular apoptotic machinery in the cytoplasm to inhibit TNF-alpha-induced apoptosis. ERbeta also interacts with components of the cytoplasmic inflammasome to increase interleukin-1beta and thus enhance its cellular adhesion and proliferation properties. Furthermore, this gain of ERbeta function enhances epithelial-mesenchymal transition signaling, thereby increasing the invasion activity of endometriotic tissues for establishment of ectopic lesions. Collectively, we reveal how endometrial tissue generated by retrograde menstruation can escape immune surveillance and develop into sustained ectopic lesions via gain of ERbeta function. |
