Kaufmann Peter, Black Simon, Huppertz Berthold
Department of Anatomy II, University of Technology Aachen, D-52057 Aachen, Germany.
Biol Reprod. 2003 Jul;69(1):1-7. doi: 10.1095/biolreprod.102.014977. Epub 2003 Mar 5.
Maternal uteroplacental blood flow increases during pregnancy. Altered uteroplacental blood flow is a core predictor of abnormal pregnancy. Normally, the uteroplacental arteries are invaded by endovascular trophoblast and remodeled into dilated, inelastic tubes without maternal vasomotor control. Disturbed remodeling is associated with maintenance of high uteroplacental vascular resistance and intrauterine growth restriction (IUGR) and preeclampsia. Herein, we review routes, mechanisms, and control of endovascular trophoblast invasion. The reviewed data suggest that endovascular trophoblast invasion involves a side route of interstitial invasion. Failure of vascular invasion is preceded by impaired interstitial trophoblast invasion. Extravillous trophoblast synthesis of nitric oxide is discussed in relation to arterial dilation that paves the way for endovascular trophoblast. Moreover, molecular mimicry of invading trophoblast-expressing endothelial adhesion molecules is discussed in relation to replacement of endothelium by trophoblast. Also, maternal uterine endothelial cells actively prepare endovascular invasion by expression of selectins that enable trophoblast to adhere to maternal endothelium. Finally, the mother can prevent endovascular invasion by activated macrophage-induced apoptosis of trophoblast. These data are partially controversial because of methodological restrictions associated with limitations of human tissue investigations and animal studies. Animal models require special care when extrapolating data to the human due to extreme species variations regarding trophoblast invasion. Basal plates of delivered placentas or curettage specimens have been used to describe failure of trophoblast invasion associated with IUGR and preeclampsia; however, they are unsuitable for these kinds of studies, since they do not include the area of pathogenic events, i.e., the placental bed.
孕期母体子宫胎盘血流量增加。子宫胎盘血流改变是异常妊娠的核心预测指标。正常情况下，子宫胎盘动脉被血管内滋养层侵入，并重塑为扩张的、无弹性的管道，不受母体血管舒缩控制。重塑紊乱与子宫胎盘血管高阻力的维持以及宫内生长受限（IUGR）和先兆子痫有关。在此，我们综述血管内滋养层侵入的途径、机制及调控。综述数据表明，血管内滋养层侵入涉及间质侵入的一条旁侧途径。血管侵入失败之前存在间质滋养层侵入受损。探讨了绒毛外滋养层一氧化氮的合成与为血管内滋养层铺平道路的动脉扩张的关系。此外，还讨论了表达内皮黏附分子的侵入性滋养层的分子模拟与滋养层取代内皮的关系。而且，母体子宫内皮细胞通过表达选择素积极准备血管内侵入，使滋养层能够黏附于母体内皮。最后，母体可通过活化巨噬细胞诱导的滋养层凋亡来阻止血管内侵入。由于与人体组织研究和动物研究局限性相关的方法学限制，这些数据存在部分争议。由于滋养层侵入在物种间差异极大，将动物模型数据外推至人类时需格外谨慎。已使用分娩胎盘的基底板或刮宫标本描述与IUGR和先兆子痫相关的滋养层侵入失败；然而，它们不适用于此类研究，因为它们不包括致病事件发生的区域，即胎盘床。
