Leptin inhibits decidualization and enhances cell viability of normal human endometrial stromal cells.

Recent reports have demonstrated that the peritoneal fluid and serum concentrations of leptin are increased in women with endometriosis. However, the pathophysiological roles of leptin in endometriosis have not been well characterized. In this study, we examined the direct effects of leptin on normal human endometrial stromal cells using an in vitro decidualization assay system with 8-Br-cAMP, a decidualization inducer. No effects of leptin on cell viability and prolactin secretion were found in unstimulated endometrial stromal cells. Leptin dose-dependently enhanced the viability of stromal cells co-stimulated with 8-Br-cAMP and leptin while PRL secretion from the cells was significantly inhibited in a dose-dependent manner. As for 8-Br-cAMP-stimulated cells, leptin significantly enhanced their cell viability in a dose-dependent manner but not their PRL secretion. These results indicate that leptin enhances the cell viability of PRL-non-secreting 8-Br-cAMP-stimulated stromal cells, and that it inhibits the decidualization process of endometrial stromal cells. Increased leptin in endometriotic patients might play an antiapoptotic role in some activated ESCs in the peritoneal cavity to stimulate endometrial cell implantation, and might cause infertility by inhibiting stromal decidualization.