中文摘要（限400字）：目前，女性不孕、流产、子宫内膜异位等疾病逐年增多，已成为亟待解决的重大问题。而这些疾病多与妊娠早期事件异常有关。因此，揭示妊娠早期胚胎植入并与母体建立稳定联系的分子机制，找出其中的关键环节，就成为解决问题的关键。酪氨酸磷酸酶Shp2 是一个重要的细胞信号调控分子，我们在小鼠子宫上皮细胞和基质细胞同时敲除它时，发现子宫接受态被破坏，雌激素信号受阻；但这种缺陷是由于某一种细胞内Shp2缺失，还是两种细胞Shp2缺失共同造成？Shp2缺失是否影响子宫蜕膜化？Shp2是如何调控两种细胞的信号及介导它们的互动？为了明确这些问题，本申请课题在子宫上皮细胞或基质细胞分别敲除Shp2，从不同方向研究Shp2在妊娠早期事件中的作用及机制，通过对Shp2整体调控作用的理解，揭示妊娠早期子宫各类型细胞互动的信号调控机制，找出其中的关键环节，为理解和治疗妊娠早期事件异常的疾病提供理论支持。

At present, female reproductive diseases, such as infertility, miscarriage and endometriosis, are increasing year by year, and have become a major problem to be solved. Because these diseases are related to abnormal events in early pregnancy, the key to solve the problem is to reveal how embryo establishes stable relations with the mother in early pregnancy, and find out the key link in these processes. Tyrosine phosphatase Shp2 is an important part of the cell signal transduction molecules. Our previous studies found deletion of Shp2 both in the uterine epithelial cells and stromal cells of mice destroyed the establishment of uterus receptive state and blocked the estrogen signaling pathway. But are the defects due to the insufficient of Shp2 in one or two types of cell? Does Shp2 influence uterine decidua? How does Shp2 mediate the interaction between the uterine epithelial cells and stromal cells? To clear these questions, this application subject will research the regulation of Shp2 and the underlying mechanism in the early pregnancy by deleting Shp2 in uterine epithelial cells or stromal cells, respectively. The results will promote understanding of the signaling network in the interaction between cells in early pregnancy, find out the key step, and provide theoretical support for early pregnancy diseases.