Study summary · research use only
Mechanism of human chorionic gonadotropin in endometrial receptivity via the miR-126-3p/PI3K/Akt/eNOS axis
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study, using an embryo implantation dysfunction (EID) mouse model established with mifepristone and human endometrial epithelial cells (EECs), examined human chorionic gonadotropin (hCG) effects on endometrial receptivity via the miR-126-3p/PIK3R2/PI3K/Akt/eNOS pathway. Researchers measured CD105 expression and CD144/CD146 protein levels by immunohistochemistry and Western blot, along with miR-126-3p, PIK3R2, and pathway protein levels, and assessed cell proliferation by CCK-8 and EdU assays. hCG treatment was associated with increased miR-126-3p and decreased PIK3R2 in EID mice and EECs, and with increased EEC proliferation, which was reduced when miR-126-3p was downregulated. The authors report that hCG activated the PI3K/Akt/eNOS pathway through the miR-126-3p/PIK3R2 axis in both the mouse and cell models.
Abstract
Human chorionic gonadotropin (hCG) might affect endometrial receptivity, exerting integral roles in embryo implantation. This study explored the action of hCG in endometrial receptivity via the miR-126-3p/PIK3R2/PI3K/Akt/eNOS axis. The embryo implantation dysfunction (EID) mouse models were established by administrating mifepristone and human endometrial epithelial cells (EECs) were used for in vivo experiments, both followed by hCG treatment. Expression level of CD105 and protein levels of cadherin CD144 and CD146 in mice were determined by immunohistochemistry and Western blot. The levels of miR-126-3p and PIK3R2 mRNA and PIK3R2, p-PI3K p85 α, PI3K p110 α, p-Akt, Akt, p-eNOS, and eNOS protein levels were measured. Cell proliferation was evaluated by CCK-8 and EdU assays. The binding sites of miR-126-3p and PIK3R2 were predicted and verified. hCG-treated EECs were further transfected with miR-126-inhibitor for functional rescue experiments. hCG ameliorated endometrial receptivity in EID mice. Moreover, hCG promoted miR-126-3p and suppressed PIK3R2 in EID mice and EECs. miR-126-3p targeted PIK3R2. EEC proliferation was enhanced after hCG treatment but inhibited by miR-126-3p downregulation. Both in vivo and in vitro experiments validated that hCG activated the PI3K/Akt/eNOS pathway through the miR-126-3p/PIK3R2 axis. Collectively, hCG improves endometrial receptivity by activating the PI3K/Akt/eNOS pathway via regulating miR-126-3p/PIK3R2.
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