子宫螺旋动脉重铸与病理妊娠

Uterine Spiral Artery Remodeling and Pathology Pregnancy

子宫螺旋动脉重铸是妊娠正常进行的关键环节,绒毛外滋养细胞的增殖和侵袭是血管重铸过程的必要条件。滋养细胞生物学功能的完整和调控机制的协调起着至关重要的作用。滋养细胞浸润不足,栓塞螺旋动脉不彻底,母-胎循环的发生提前,使绒毛受到直接的机械损伤,氧化应激作用间接地造成细胞机能障碍和损伤,出现胎盘退化变性;人肿瘤蛋白p53(TP53)介导细胞通路对细胞周期蛋白依赖性激酶抑制剂1A(CDKN1A)和Bax基因的异常表达,微小RNA-520(miR-520)过度调控滋养细胞的凋亡导致母体出现复发性流产。由滋养细胞分泌产生的基质金属蛋白酶9(MMP-9)的异常表达和大量炎性因子的释放造成了胎盘缺血缺氧,表现出子痫前期的相关症状。胎盘绒毛的血管密度、绒毛间隙体积的降低、滋养细胞分化程度下降、微环境缺氧以及突触缺陷因子1(SYDE1)呈低水平表达,可能是造成胎儿生长受限的重要原因。因此研究螺旋动脉重铸过程对病理妊娠的早期诊治有着重要意义。

Uterine spiral artery remodeling is the key procedure in normal pregnancy. The proliferation and invasion of trophoblast cells is necessary for vascular remodeling process. When the trophoblast invasion is not fully enough, the spiral artery embolism is uncomplete, maternal-fetal circulation occurs earlier, the villi are damaged mechanically and directly.Oxidative stress cause cellular dysfunction and injury indirectly, followed by placental degeneration; cyclin-dependent kinase inhibitor 1A（CDKN1A） and Bax gene expressing abnormally caused by the pathway mediated TP53 protein, the apoptosis of trophoblast over regulated by miR-520 may lead to the emergence of the recurrent spontaneous abortion. The abnormal expression of MMP-9 produced by trophoblast cells and the release of a large number of inflammatory factors cause placental ischemia and hypoxia. The decrease of the vascular density, the volume of villus space, the degree of differentiation of trophoblast cells,hypoxia in microenvironment and the low level expression of synapse defective 1（SDYE1） in placental villi may be an important cause of fetal growth restriction. So the study of spiral artery remodeling process has important significance for early diagnosis and treatment of pathological pregnancy.