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(American Journal of Pathology. 2007;170:126-139.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060175

Expression of the Metastasis Suppressor KAI1 in Decidual Cells at the Human Maternal-Fetal Interface

Regulation and Functional Implications

Birgit Gellersen^*, Juliane Briese, Marine Oberndörfer, Katja Redlin^*, Annemarie Samalecos^*, Dagmar-Ulrike Richter, Thomas Löning, Heinrich-Maria Schulte^* and Ana-Maria Bamberger

From the Endokrinologikum Hamburg,^* Hamburg; Section on Endocrinology and Metabolism of Ageing, University Clinic Hamburg-Eppendorf, Hamburg; Department of Obstetrics and Gynecology in Klinikum Südstadt, University of Rostock, Rostock; and Reference Center for Gynecopathology and Cytology at the Institute of Pathology, University Clinic Hamburg-Eppendorf, Hamburg, Germany

At the human maternal-fetal interface, the decidua forms a dense matrix that is believed to limit trophoblast invasion. We investigated whether the metastasis suppressor KAI1 (CD82) is expressed at the maternal-fetal interface. Immunohistochemistry showed strong expression of KAI1 in decidual cells, whereas trophoblast cells were negative for KAI1. In luteal phase endometrium, KAI1 was present in decidualizing endometrial stromal cells. We investigated whether KAI1 expression in endometrial stromal cells is regulated by the decidualizing stimuli cAMP and progesterone or by the cytokine interleukin (IL)-1ß. Western blot analysis revealed induction of KAI1 protein by cAMP analog, but not by progesterone, in a delayed fashion. In contrast, IL-1ß rapidly stimulated KAI1 expression at the transcript level and at the protein level. Cultured decidual cells from term placenta expressed a basal level of KAI1 protein that was elevated on cAMP stimulation. Silencing of KAI1 by RNA interference attenuated expression of decorin, a decidual product implicated in limiting trophoblast invasion. This study shows for the first time the expression of KAI1 in decidual cells at the human maternal-fetal interface, where the metastasis suppressor might participate in intercellular communication with trophoblast cells and the control of trophoblast invasion.

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