蛋白质O-GlcNAc糖基化修饰广泛参与基因表达、细胞周期、细胞骨架维持，在胚胎发育与着床调控作用尚趋空白。SP1存在多个O-GlcNAc修饰位点，申请人前期明确SP1靶向AQP3表达参与子宫内膜细胞侵袭、迁移。本研究①明确O-GlcNAc修饰对小鼠胚胎发育、着床能力的影响；②明确O-GlcNAc修饰与子宫内膜接受状态建立的相关性；③调控O-GlcNAc修饰分析对生长因子、EMT分子、血管生成分子表达及对胚胎与子宫内膜黏附、侵袭及胎盘功能的影响；④确定Sp1的O-GlcNAc修饰活性的精确位点；分析Sp1对子宫内膜AQP3动态表达影响能否引起甘油堆积并引起子宫内膜能量摄入及代谢方式的变化；⑤检测Ogt条件基因敲除小鼠生殖能力；逐步揭示O-GlcNAc修饰调控滋养层细胞与子宫内膜基质结合、内膜蜕膜化、血管重塑等过程的分子机制，为临床子痫前期及滋养细胞肿瘤的妊娠疾病的防治提供理论依据。

O-GlcNAc glycosylation modification is widely involved in regulating gene expression, cellcycle, cytoskeleton maintenance, etc., and its role in embryonic development and implantation is still unknown. We determined that SP1 which there were multiple O-GlcNAc modification sites targeting AQP3 expressionwasinvolved in the invasion and migration of endometrial cells. In this research,we will explore ①the effect of O-GlcNAc modification on mouse embryo development and implantation;②the correlation between O-GlcNAc modification and establishment of the uterineendometrial receptivity ; ③effect of O-GlcNAc modulation on the SP1, growth factor, EMT molecule, angiogenesis expression ,embryo adhesion and invasionin endometrium, and the function of placenta; ④confirming the accurate site of O-GlcNAc modification of SP1, analizing the effect on AQP3 and it can causeglycerol accumulation and changes of energy intake and metabolismin endometrial;⑤detecting the reproductive ability in Ogt conditional knockout mouse and clarify the molecular mechanism of O-GlcNAc modification regulating the binding between trophoblast cells and endometrial stroma, endometrial decidualization, vascular remodeling and others processeswhich will provide the theoretical basis for treatment and prevention of pregnancy-related diseases with preeclampsia and trophoblastic tumorin clinic.