| 【Background】Preeclampsia is one of the serious complications of pregnancy and remains the main cause of maternal mortality and adverse perinatal outcomes.Preeclampsia belongs to placental diseases,mainly caused by dysfunction and involving multiple systems.In the past,a large number of studies have focused on the aspect of villous trophoblasts,but the placenta is an important bridge connecting the mother and fetus.During the formation and normal development of the placenta,it needs to coordinate and develop with the uterine decidua.The decidualization defect can change the microenvironment of the maternal fetal interface,leading to abnormal placental function,and ultimately inducing adverse pregnancy outcomes such as pre eclampsia.However,the specific mechanism leading to abnormal decidualization in preeclampsia is still unclear and further exploration is needed.【 Objective 】 Exploring the impact of abnormal expression of MeCP2 on the decidualization of human endometrial stromal cells and the pathogenesis of preeclampsia.【 Mecthods 】 Immunohistochemistry,real-time fluorescence quantification,and protein immunoblotting were used to determine the expression of MeCP2 in human decidual tissue;Constructing a decidualization model using human endometrial stromal cells(hESC)in vitro to observe the changes of MeCP2 during decidualization;Construct an hESC model of knockdown MeCP2 and observe its impact on the decidualization process.【Results】Compared with mothers with normal pregnancy outcomes,the expression of MeCP2 m RNA and protein levels in the decidual tissue of preeclampsia patients significantly decreased;Knocking down MeCP2 reduces the ability of human endometrial stromal cells to induce decidualization.【Conclusion】The expression of MeCP2 related molecules decreases in pre eclampsia decidual tissue,while downregulating the expression of FOXO1,affecting endometrial decidual transformation,and inhibiting the expression of IGFBP1. |
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