| Literature DB >> 26544941 |
Sang Jun Han1, Sung Yun Jung2, San-Pin Wu1, Shannon M Hawkins3, Mi Jin Park1, Satoru Kyo4, Jun Qin2, John P Lydon1, Sophia Y Tsai1, Ming-Jer Tsai1, Francesco J DeMayo1, Bert W O'Malley5.
Abstract
Alterations in estrogen-mediated cellular signaling play an essential role in the pathogenesis of endometriosis. In addition to higher estrogen receptor (ER) β levels, enhanced ERβ activity was detected in endometriotic tissues, and the inhibition of enhanced ERβ activity by an ERβ-selective antagonist suppressed mouse ectopic lesion growth. Notably, gain of ERβ function stimulated the progression of endometriosis. As a mechanism to evade endogenous immune surveillance for cell survival, ERβ interacts with cellular apoptotic machinery in the cytoplasm to inhibit TNF-α-induced apoptosis. ERβ also interacts with components of the cytoplasmic inflammasome to increase interleukin-1β and thus enhance its cellular adhesion and proliferation properties. Furthermore, this gain of ERβ 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 ERβ function.Entities:
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Year: 2015 PMID： 26544941 PMCID： PMC4640214 DOI： 10.1016/j.cell.2015.10.034
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582