子宫内膜异位症（Endometriosis，EM）是育龄妇女多发病常见病,与多种产科并发症尤其是前置胎盘密切相关，危害母儿，机制不清。孕激素在整个妊娠过程中发挥核心作用，而EM患者因孕激素受体亚型表达量及比例异常而普遍存在孕激素抵抗。子宫内膜-肌层交界区（endometrial-myometrial interface，EMI）理论的兴起有力解释EM的发病机制，并有可能在前置胎盘发病机制中开辟新的篇章。我们认为内异症EMI区域孕激素受体及其下游产物的异常,影响了EMI蠕动的方向和强度，并进一步导致着床部位下移而形成前置胎盘，从该角度去解释其发病机制国内外尚无报道。本研究拟通过大鼠内异症妊娠动物模型了解其EMI区域孕激素受体表达，并进一步临床验证孕激素和EMI功能的改变及前置胎盘相关性。该研究有助于阐明EM相关前置胎盘的发病机制，并对该病的预防以及新的治疗药物开辟新的思路。

Endometriosis, a common disease in women of child-bearing age, has close relationship with many obstetric complications especially placenta praevia. It has been well documented to be associated with adverse maternal outcomes as well as neonatal outcomes, consuming large amounts of health resources. However, the pathogenesis is still unclear. Progesterone plays a major role to prepare the uterus for implantation and in the establishment and maintenance of pregnancy. There is widespread progesterone resistance in endometriosis, due to the abnormal expression of PR subtypes and other downstream products. With the improvement of medical imaging, a more complex spatial and functional units was denominate as endometrial-myometrial interface(EMI), which develop into “tissue injury and repair(TIAR)” theory. It explains both endometriosis and adenomyosis and might offer a new way explain placenta praevia. We supposed that changes of progesterone receptors in EMI will cause dysperistalsis, which might effect the implantation and makes placenta moving forward to cervix. To our knowledge, few studies have been performed on this before. In this study, we will first detect the expression of progesterone receptors in pregnant rats with endometriosis; secondly, the relationship between progsterone,EMI function and placenta previa will be testified clinically. Our study will provide new insights into the mechanisms underlying endometriosis associated placenta previa, thus opening new potential avenues for both prevention and treatment.

子宫内膜异位症（Endometriosis，EM）是育龄妇女多发病常见病,与多种产科并发症尤其是前置胎盘密切相关，危害母儿，消耗大量卫生资源，机制不清。孕激素在整个妊娠过程中发挥着核心作用，而EM患者普遍存在孕激素抵抗,与孕激素受体亚型表达量及比例改变从而引起下游产物异常表达相关。子宫内膜-肌层交界区（endometrial-myometrial interface，EMI）理论的兴起有力的解释了EM的发病机制，并有可能在前置胎盘发病机制中开辟新的篇章。该研究首先通过临床数据的总结证实了内异症患者前置胎盘发病率增加的现象，进一步通过超声影像学发现EMI区域在孕期蠕动的减弱调整了孕期子宫平滑肌的收缩。在动物实验方面，首先成功建立了内异症妊娠大鼠模型，获取宝贵的不同孕期EM大鼠及非EM大鼠子宫平滑肌组织，提取RNA并研究其孕激素受体及下游收缩离子通道子表达，发现表达差异的因子，从而解释EM孕产妇EMI功能异常及前置胎盘的发病机制，并进一步外源性应用孕激素并了解相关因子的改变，探索其预防和治疗机制。