Regulation mechanism of miR-494-3p on endometrial receptivity in mice via PI3K/AKT/mTOR pathway

Successful implantation requires endometrial receptivity. To investigate the mechanisms of miR-494-3p on receptivity, GnRHa's superovulation scheme was designed to reduce and pregnant mice were injected with antagomir. The regulatory role identified by RT-qPCR, uterine blastocyst count, scanning electron microscopy, hematoxylin-eosin (HE) staining, Western blot. Results indicated that antagomir increased blastocysts numbers, promoted pinocytosis expressions, thickness. Besides, significantly leukemia inhibitory factor (LIF), Ang-2 VEGF protein up-regulated p-AKT/AKT p-mTOR/mTOR ratios in endometrium. Luciferase assay confirmed LIF a potential target miR-494-3p. Subsequently, human epithelial cells (hEECs) transfected inhibitor PI3K (LY294002). CCK-8 assay, transwell flow cytometry. proliferation invasion, inhibited apoptosis hEECs, while LY294002 reversed its biological function. Overall, these results suggested is key regulator receptivity mice, regulating this complex process through PI3K/AKT/mTOR pathway. Understanding great significance for exploring new targets diagnosis treatment early pregnancy failure, improving success rates artificial reproduction.