Interaction of Jar choriocarcinoma cells with endothelial cell monolayers.

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.