mTOR signaling and endometrial receptivity in infertile women with intramural uterine leiomyomas

Abstract Background Receptive endometrium is a restraining factor in the establishment of pregnancy several estrogen-dependent gynecological disorders including uterine leiomyomas. Recently, data are beginning to accrue suggesting negative impact non-cavity distorting intramural fibroids on molecular mediators endometrial receptivity. The potential importance mammalian target rapamycin (mTOR) signaling pathway has been suggested during embryo implantation. However, its exact role fibroid-associated window implantation poorly defined. objective study was examine expression and cellular distribution key components mTOR infertile women with leiomyomas ( n = 24) as compared fertile controls 17). Relative gene analysis , TSC1 TSC2 performed by real-time PCR. Immunohistochemistry used evaluate mTOR, phospho-mTOR (Serine 2448), TSC1, TSC2, phospho-TSC2 (Threonine 1462), phospho-S6 ribosomal protein (Serines 235 236) Ki67. Results In comparison controls, statistically significant upregulation (8.97-fold; p < 0.001) downregulation mRNA (− 6.01-fold; 0.01) levels cell-specific proteins phospho-mTOR, phospho-TSC2, were observed women. ratio p-mTOR/mTOR p-TSC2/TSC2 significantly higher Pearson’s correlation revealed between p-mTOR positive p-S6 group. Increased Ki67 labelling index glandular epithelium (GE) stroma from controls. Conclusions Loss function enhanced activated downstream targets, group, indicate heightened which might contribute impaired number Ki67-positive nuclei suggests that may help drive dysregulated proliferation midsecretory leading compromised fertility present findings provide avenues for future investigation nonsurgical alternative treatment infertility these patients.