ORIGINAL ARTICLE: Trophoblasts and Shear Stress Induce an Asymmetric Distribution of ICAM-1 in Uterine Endothelial Cells
Article first published online: 24 OCT 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Munksgaard
American Journal of Reproductive Immunology
Volume 59, Issue 2, pages 167–181, February 2008
How to Cite
Cao, T. C., Thirkill, T. L., Wells, M., Barakat, A. I. and Douglas, G. C. (2008), ORIGINAL ARTICLE: Trophoblasts and Shear Stress Induce an Asymmetric Distribution of ICAM-1 in Uterine Endothelial Cells. American Journal of Reproductive Immunology, 59: 167–181. doi: 10.1111/j.1600-0897.2007.00542.x
- Issue published online: 24 OCT 2008
- Article first published online: 24 OCT 2008
- Submitted July 26, 2007; accepted September 18, 2007.
- Adhesion molecule;
Problem We have used an in vitro co-culture system consisting of early gestation macaque trophoblasts cultured on top of human uterine microvascular endothelial cells (UtMVECs) to investigate the inflammatory response of endothelial cells to trophoblasts under shear stress conditions.
Method of study Uterine microvascular endothelial cells and trophoblasts were co-cultured in a parallel plate chamber under shear stress (15 dyn/cm2) conditions. The distribution and expression of endothelial intercellular adhesion molecule-1 (ICAM-1) was quantified by immunofluorescence image analysis and flow cytometry. Endothelial regulated upon activation normal T-cell expressed and secreted (RANTES) secretion was measured by enzyme-linked immunosorbent assay and permeability was assessed using fluorescein isothiocyanate-dextran.
Results Intercellular adhesion molecule-1, but not vascular cell adhesion molecule-1 or platelet endothelial cell adhesion molecule-1, was re-distributed towards the downstream edge of endothelial cells when the cells were co-cultured with trophoblasts under shear stress conditions. Changes in ICAM-1 distribution were also observed when UtMVECs were co-cultured with trophoblast-conditioned medium under shear stress conditions. Incubation of UtMVECs with trophoblast-conditioned medium increased endothelial permeability, RANTES secretion, and trophoblast adhesion.
Conclusion These data support the idea that trophoblasts induce an inflammatory response in uterine endothelial cells that could enhance trophoblast invasion and transmigration.