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Expression of Na⁺/I^- Symporter and Pendred Syndrome Genes in Trophoblast Cells¹

Departments of Clinical Biology (J.M.B., L.L., V.L., D.B.), Pathology (B.C.), and Nuclear Medicine (M.S.), Institut Gustave-Roussy, 94805 Villejuif, France; INSERM U-427 (D.E.-B.), Laboratoire d’Immunologie des Tumeurs, ESA 8067, Centre National de la Recherche Scientifique (J.M.B., D.B.), Faculté des Sciences Pharmaceutiques et Biologiques, Université René Descartes, 75006 Paris, France; Service de Gynécologie Obstétrique, Hôpital Antoine Béclère (R.F.), 92141 Clamart, France; and Dipartimento di Medicina Sperimentale e Clinica, Policlinico Mater Domini (S.F.), 88100 Catanzaro, Italy

Address all correspondence and requests for reprints to: Dr. J. M. Bidart, Institut Gustave-Roussy, 39 rue Camille Desmoulins, 94805 Villejuif, France. E-mail: bidart{at}igr.fr

Placental iodide transport is critical for the fetal thyroid function, but the molecular mechanisms of this transport are not understood. The expression of two recently identified iodide transporters, namely the sodium/iodide symporter (NIS) and pendrin, the product of the gene responsible for the Pendred syndrome (PDS), was studied using real-time kinetic quantitative PCR and immunohistochemistry 1) in placental tissues collected at different gestational ages and 2) in primary cultures of villous cytotrophoblast cells (VCT) that differentiate and fuse over 2–3 days in vitro to form villous syncytiotrophoblast (VSCT) cells.

Both NIS and PDS genes are expressed in placenta, albeit at low levels compared with those in thyroid tissue. NIS gene expression in placental samples from first trimester and term pregnancies was similar. In contrast, the expression of PDS gene was higher in term than in first trimester pregnancy samples. In vitro, NIS gene was expressed at a high level in VCT obtained from first trimester pregnancy, and its expression decreased by 3- to 4-fold during the differentiation of VCT in VSCT. Expression of NIS was lower (up to 30-fold) in VCT obtained in placental samples from third trimester than from first trimester pregnancy. In contrast, the expression of PDS gene was low in VCT and increased by 5- to 10-fold during VSCT formation; this was observed in cells isolated from placental samples of both first trimester and term pregnancies. Immunohistochemical analysis showed that NIS protein was present on the entire membrane of VCT, whereas pendrin was mainly located at the brush border membrane of VSCT, facing the mother. In conclusion, 1) NIS and PDS genes are differently expressed in the placenta during gestation; and 2) whereas pendrin is expressed at the brush border membrane of syncytiotrophoblast cells, NIS protein is mainly located in the cytotrophoblast layer.

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