Activated endothelial cells resist displacement by trophoblast in vitro.
BACKGROUND
Transformation of the spiral arteries by invading trophoblasts is an essential prerequisite to the development of a healthy fully grown fetus. Reduced transformation of the spiral arteries is a characteristic feature of pregnancies complicated by several diseases of pregnancy including preeclampsia. The aim of this study was to investigate further the hypothesis that spiral artery endothelial cells can contribute to the mechanism of shallow trophoblast invasion.


METHODS
Fluorescently labeled Jar cells were added to monolayers of fluorescently-labeled endothelial cells that had been activated by treatment with TNFalpha, INF gamma or necrotic cell bodies. The ability of the Jars to displace endothelial cells from the monolayers was quantified by measuring the area of Jar cells "islands" formed in the endothelial cell monolayers by confocal microscopy and digital image.


RESULTS
The area of Jar cell islands formed in monolayers of activated endothelial cells was significantly smaller that the area of islands formed in control resting/non-activated endothelial cell monolayers regardless of the activator.


CONCLUSIONS
This work demonstrates that activated endothelial cells are more resistant to trophoblast displacement than resting endothelial cells and adds weight to the suggestion that endothelial cells could contribute to shallow invasion of the spiral arteries by trophoblasts in diseases such as preeclampsia.
Chen
Q
Q
Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, The University of Auckland, 85 Park Road, Grafton, Auckland 1001, New Zealand. q.chen@auckland.ac.nz
Stone
P R
PR
McCowan
L M E
LM
Chamley
L W
LW
D002460:Cell Line; D018920:Coculture Techniques; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D014327:Trophoblasts / Q000166:cytology / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma