Regulation of SIRT1 determines initial step of endometrial receptivity by controlling E-cadherin expression.

摘要: Sirtuin 1 (SIRT1), originally found as a class III histone deacetylase, is principal modulator of pathways downstream calorie restriction, and the activation SIRT1 ameliorates glucose homeostasis insulin sensitivity. We examined role in regulation uterine receptivity using Ishikawa RL95-2 endometrial carcinoma cell lines. Exogenous expression significantly enhanced E-cadherin expression, while small interfering RNA-mediated depletion endogenous resulted significant reduction expression. A activator resveratrol elevated dose dependent manner, repressors nicotinamide sirtinol exhibited also showed that both forced promote E-cadherin-driven reporter gene constructs, localized at promoter containing E-box elements cells. Using an vitro model embryo implantation, we demonstrate exogenous stimulation activity line becoming receptive to JAR spheroid attachment. Furthermore, Glycodelin protein sites intercellular contact, suggesting additive promoting implantation. The initial step human reproduction depends on capacity attach implant into wall, these results revealed novel mechanism increased play important receptivity.