Fludrocortisone improves endometrial receptivity by regulating expression of ENaC, SGK1, HAND2, miR-200a, miR-145, miR-451, mTOR, and 4E-BP1 during the implantation window in mice

This study investigated the effect of fludrocortisone treatment on the expression of genes and proteins involved in the implantation process in mice.

The study involved four groups of mice, and mRNA and protein expression were measured using real-time PCR and western blotting.

The results showed that fludrocortisone treatment slightly downregulated the expression of SGK1, ENaC-α, miR-145, and miR-200a, while slightly upregulating the expression of HAND2, miR-451, mTOR, and 4E-BP1 in the endometrial epithelium. mTOR kinase inhibitor PP242 treatment resulted in the upregulation of miR-145 and miR-200a, while partially downregulating the expression of p-4E-BP1, mTOR, SGK1, ENaC-α, HAND2, and miR-451 expression. Combination therapy of fludrocortisone and PP242 resulted in slightly decreased expression of ENaC, SGK1, miR-200a, miR-145, and 4E-BP1, while slightly upregulating the expression of miR-451 and HAND2 in the epithelial endometrium.

The findings indicated that fludrocortisone did not disrupt endometrial receptivity and may even enhance it by modulating gene expression through the activation of the mTOR signaling pathway. Overall, the study suggests that fludrocortisone treatment can modulate the expression of genes and proteins involved in the implantation process in mice. The activation of the mTOR signaling pathway was also increased during the treatment. The findings indicate that fludrocortisone may increase endometrial receptivity without disrupting it, which could have implications for fertility treatment.