Regulation of trophoblast invasion: from normal implantation to pre-eclampsia
Regulation of trophoblast invasion: from normal implantation to pre-eclampsia
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DOI：
10.1016/s0303-7207(01)00687-6
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发表时间：
2002-02-22
影响因子：
4.1
通讯作者：
Yagel, S
中科院分区：
文献类型：
--
作者：
Goldman-Wohl, D;Yagel, S
母体螺旋动脉转变为较大的主管血管是正常胎盘发育的重要步骤之一。这一过程显然依赖于子宫内膜下区域滋养细胞和螺旋动脉的侵入。先兆子痫的特征是滋养层浸润较浅，螺旋状动脉狭窄。这导致胎儿缺氧，导致内皮损伤，最终表现为母体高血压。水肿和蛋白尿。以下步骤已被证明涉及滋养层从子宫腔进入蜕膜和螺旋动脉的突破：滋养层靶向，粘附和脱离细胞外基质（ECM）。通过蛋白水解侵入ECM和母体血管。这些分子的异常表达和活性可以部分解释导致异常胎盘形成和先兆子痫发生的分子机制。(C)2002爱思唯尔科学爱尔兰有限公司保留所有权利。
Conversion of the maternal spiral arteries into larger competent vessels is one of the essential steps in the development of the normal placenta. This process is apparently dependent on the invasion by trophoblasts of the sub-endometrial area and the spiral arteries. Preeclampsia is characterized by shallow, trophoblast invasion and unconverted narrow, spiral arteries. This leads to fetal hypoxia that causes endothelial injury that eventually manifest as maternal hypertension. edema, and proteinuria. The following steps have been shown to be involved in the breakthrough of the trophoblasts from the uterine cavity into the decidua and the spiral arteries: trophoblast targeting, adhesion, and detachment from the extracellular matrix (ECM). invasion of the ECM and maternal vessels by proteolysis. Abnormal expression and activity of these molecules may explain in part some of the molecular mechanisms leading to abnormal placentation and the development of preeclampsia. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.