早产是导致围产期新生儿发病和死亡的主要原因，而未足月胎膜早破(pPROM)是早产发生的主要原因。研究报道pPROM的羊水成分发生异常并可导致羊膜上皮细胞功能紊乱。外泌体作为介导细胞通讯的重要媒介被报道参与多项生理及病理过程。研究发现pPROM羊水中的外泌体携带特异表达的蛋白，但其是否调控羊膜上皮细胞的功能并参与pPROM的发生尚不得而知。针对这一问题，我们前期研究发现pPROM羊水外泌体抑制羊膜上皮细胞的增殖和迁移，促进其凋亡。但羊水外泌体及差异蛋白对羊膜上皮细胞的调控机制及下游信号通路尚不明确。因此，本项目围绕羊水中的外泌体，检测pPROM羊水外泌体差异表达的蛋白，通过RNA-seq和信号通路高通量蛋白芯片确定差异蛋白的下游靶基因及信号通路，并利用小鼠模型明确pPROM羊水外泌体中的特异蛋白在引发pPROM中的关键作用，旨在发现pPROM发生的新机制，为预防pPROM提供充分的理论依据。

Preterm birth is the leading cause of morbidity and mortality in perinatal neonates, and preterm premature rupture of the membranes (pPROM) is considered to be the main cause of preterm birth. It is reported that aberrant amniotic fluid component of pPROM can lead to dysfunction of amniotic epithelial cells. Exosomes participate in a number of physiological and pathological processes as an important mediator of cell-to-cell communication. Studies have found that in pPROM amniotic fluid exosomes carry specific proteins, but whether exosomes regulate the function of amnion epithelial cells in pPROM is unclear. To investigate this problem, our previous study found that in pPROM amniotic fluid exosomes inhibit the proliferation and migration of amnion epithelial cells and promote apoptosis. However, the mechanism of amniotic fluid-derived exosomes regulating amniotic epithelial cells function still remain elusive up to now. Therefore, this project will detect specific proteins in amniotic fluid-derived exosomes, identify downstream signal pathways and targets regulated by specific proteins using RNA-seq and protein chips, and clarify the function of amniotic fluid-derived exosomes in the development of pPROM by using mouse model in vivo. So this study will not only explore the causes of pPROM, but also provide theoretical basis for clinical prevention of pPROM.