Interaction of Jar choriocarcinoma cells with endothelial cell monolayers
Interaction of Jar choriocarcinoma cells with endothelial cell monolayers
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DOI：
10.1016/j.placenta.2004.09.014
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发表时间：
2005-09-01
期刊：
影响因子：
3.8
通讯作者：
Chamley, LW
中科院分区：
文献类型：
--
作者：
Chen, Q;Stone, PR;Chamley, LW
在人类妊娠期间，子宫螺旋动脉被胎盘滋养层细胞侵入，胎盘滋养层细胞取代了衬在非妊娠螺旋动脉上的内皮细胞，并将这些血管转化为大口径导管，使得母体血液能够充分灌注胎盘。该过程的失败可能易患先兆子痫和胎儿生长受限[Brosens I，Robertson WB，狄克逊HG.胎盘床血管对正常妊娠的生理反应。病理学和细菌学杂志1967;93：569-79; Khong TY，De Wolf F，Robertson WB，Brosens I.妊娠合并先兆子痫和小于胎龄儿时母体血管对胎盘形成反应不足英国妇产科杂志1986;93：1049-59]。关于母体内皮细胞在这一过程中的作用的数据很少。在这项研究中，我们研究了滋养层来源的Jar细胞和内皮细胞（HUVEC和HMEC-1）之间的细胞相互作用。共聚焦显微镜、DNA片段化分析和流式细胞术检测Jar细胞与内皮细胞单层共培养的效果。我们证明了罐细胞迁移到内皮细胞单层的焦点区域，在那里它们诱导内皮细胞死亡，然后吞噬死亡的内皮细胞。我们的研究结果表明，内皮细胞可能不仅仅是被动的目标入侵滋养层细胞在重建的螺旋动脉。
During human pregnancy the uterine spiral arteries are invaded by placental trophoblasts which replace the endothelial cells that line the non-pregnant spiral arteries and transform these vessels into large-bore conduits enabling adequate perfusion of the placenta with maternal blood. Failure of this process may predispose to preeclampsia and fetal growth restriction [Brosens I, Robertson WB, Dixon HG. The physiological response of the vessels of the placental bed to normal pregnancy. Journal of Pathology and Bacteriology 1967;93:569-79; Khong TY, De Wolf F, Robertson WB, Brosens I. Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants. British Journal of Obstetrics and Gynaecology 1986;93:1049-59]. There is a paucity of data on the role of maternal endothelial cells in this process. In this study we investigated the cellular interactions between trophoblast-derived Jar cells and endothelial cells (HUVECs and HMEC-1). The effect of coculturing Jar cells with endothelial cell monolayers was determined by confocal microscopy, DNA fragmentation assay and flow cytometry. We demonstrated that Jar cells migrate into focal areas in endothelial cell monolayers, where they induce endothelial cell death and, then phagocytose the dead endothelial cells. Our results suggest that endothelial cells may not simply be passive targets for invading trophoblasts during the remodeling of the spiral arteries.