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From the Department of Gynecopathology, Institute of
Pathology,*
the Department of Clinical
Chemistry,
and the Clinic of Internal
Medicine,
University Hospital Eppendorf,
Hamburg, Germany; the Department of Obstetrics and
Gynecology,§
Alexandra Maternity Hospital,
University of Athens, Athens, Greece; the Division of Human
Reproduction,¶
Department of Obstetrics and
Gynecology and the Center for Research on Reproduction and Womens
Health, University of Pennsylvania Medical Center, Philadelphia,
Pennsylvania; and the Department of Obstetrics and
Gynecology,||
IVF Unit, Imperial College School of Science
and Medicine, Hammersmith Hospital, London, United Kingdom
CEACAM1 (CD66a, C-CAM, BGP) is an adhesion molecule of the carcinoembryonic antigen family which has been shown to be normally expressed at the apical pole of epithelial cells, including the apical pole of endometrial surface and glandular epithelia. The purpose of the present study was to investigate its expression pattern at the maternal-fetal interface, and thus to determine whether CEACAM1 could be implicated in the human implantation process. For this purpose, we performed immunohistochemistry using the 4D1/C2 monoclonal antibody (mAb) as well as flow cytometry and Western blot on isolated trophoblast populations. On the maternal side of the maternal-fetal interface, CEACAM1 was present in epithelial cells of pregnancy endometrium as well as in small endometrial vessels, whereas it was absent from decidual cells. On the fetal side, CEACAM1 was strongly expressed by the extravillous (intermediate) trophoblast at the implantation site, as well as by extravillous trophoblast cells with invasive phenotype in primary culture, as shown by flow cytometry and Western blot. Expression was also observed in placental villous core vessels but was absent from both villous cyto- and syncytiotrophoblasts throughout the pregnancy. We conclude that, given its specific expression pattern, CEACAM1 can be a useful marker for extravillous intermediate trophoblast and might be functionally implicated in mediating trophoblast/endometrial and/or trophoblast/endothelial interactions during the trophoblastic invasion of the endometrium.
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