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Osteopontin Is Colocalized with the Adhesion Molecule CEACAM1 in the Extravillous Trophoblast of the Human Placenta and Enhances Invasion of CEACAM1-Expressing Placental Cells

Institute of Pathology (J.B., M.O., C.P., T.L., A.-M.B.), University Hospital, Hamburg-Eppendorf, 20246 Hamburg, Germany; Endokrinologikum (H.M.S.), 20246 Hamburg, Germany; and Department of Obstetrics and Gynecology (A.M.), University of Iraklion, 71202 Iraklion, Greece

Address all correspondence and requests for reprints to: Juliane Briese, Institute of Pathology, University Hospital Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. E-mail: j.briese{at}uke.uni-hamburg.de.

Context: The human placenta is a complex tissue and possesses, through its capacity to proliferate and to invade maternal tissue, qualities that are usually found in malignant tumors. Osteopontin (OPN) and CEACAM1 may regulate these processes.

Objective: The present study was designed to investigate the expression pattern of OPN in the human placental components and to correlate it with CEACAM1 expression and function in placental cell invasiveness.

Design: Immunohistochemistry with an OPN-specific antibody and immunofluorescence were performed on normal placental samples to investigate the expression pattern of OPN and CEACAM1 in the human placenta. Extravillous trophoblast (EVT) hybridoma cells transfected with CEACAM1 and stimulated with OPN were studied using the Matrigel invasion assay.

Results: All placentae presented very strong expression of OPN in the EVT at the invasion front, where it colocalized with CEACAM1. In addition, OPN was also present in the villous trophoblast, with strongest expression in the cytotrophoblast of the first trimester. Transfection with CEACAM1 followed by stimulation with OPN resulted in increased invasiveness of EVT hybridoma cells.

Conclusion: The present study shows the first systematic analysis of OPN expression pattern in the human placenta showing strong expression in the EVT at the invasion front. Colocalization of OPN with CEACAM1 in the EVT indicates that they might act together to regulate invasiveness at the maternal-fetal interface. Using an in vitro model, we also demonstrated increased cellular invasiveness after OPN treatment. We speculate that OPN and CEACAM1 may act as a functional complex involved in the regulation of placental invasiveness.

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