RESUMEN
Objective:To elucidate the effect of miR-182 on proliferation, invasionof endometrial glandular epithelial cells in endometrrosis (EMs) mice via Wnt signaling pathway through targeting Aquaporin5 (AQP5) .Methods:The mice model of EMs were established. Subsequently the adenoepithelial tissue of endometrium were collected and the expression of miR-182 and AQP5 in tissue was detected. Enzyme-linked immunosorbent assay (ELISA) was performed to test the expression of inflammatory factors in normal and EMs mice. Then endometrial glandular epithelial cells in mice were isolated and divided into different groups. qRT-PCR and Western blot was performed to detect the expression of miR-182, AQP5,and Wnt pathway related factors (Wnt-1, β-catenin) in cells. The proliferation activity and invasion ability in each group of cells were examined by MTT and Transwell.Results:Compared with Normal mice, the expression of miR-182 was decreased while AQP5 and Wnt pathway related factors (Wnt-1, β-catenin) expression were increased in endometrial glandular epithelial tissues of EMs mice (all P<0.05) . In cell experiments, miR-182 overexpression or AQP5 silencing could inhibit the expression of Wnt pathway related factors (Wnt-1, β-catenin) . At the same time, cell viability as well as invasion ability were decreased (all P<0.05) . Indexes in miR-182 inhibitor group exhibited an opposite trend compared with that in miR-182 mimic group. The effects of sh-AQP5 on EMs cells could be offset by miR-182 inhibitor. Conclusion:Up-regulated expression of miR-182 can reduce the proliferation and invasion of endometrial glandular epithelial cells of EMs mice through inhibiting the activation of Wnt signaling pathway by down-regulating AQP5.