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Pendrin Is an Iodide-Specific Apical Porter Responsible for Iodide Efflux from Thyroid Cells

First Department of Internal Medicine, Tottori University Faculty of Medicine (A.Y., S.T., I.H.), Yonago, Tottori 683-8504, Japan; Genome Technology Branch, National Human Genome Research Institute (I.E.R., E.D.G.), and Cell Regulation Section, Metabolic Diseases Branch, National Institute of Digestive and Diabetes and Kidney Diseases (L.D.K., K.S.), National Institutes of Health, Bethesda, Maryland 20892-8004; Ohio University School of Osteopathic Medicine and Edison Biotechnology Institute (L.D.K.), Athens, Ohio 45701-2979; and Department of Microbiology, Leprosy Research Center, National Institute of Infectious Diseases (K.S.), Tokyo 189-0002, Japan

Address all correspondence and requests for reprints to: Dr. Akio Yoshida, First Department of Internal Medicine, Tottori University Faculty of Medicine, Nishimachi 36-1, Yonago, Tottori 683-8504, Japan. E-mail: . ayoshida{at}bronze.ocn.ne.jp

Abstract

The Pendred syndrome gene encodes a 780-amino acid putative transmembrane protein (pendrin) that is expressed in the apical membrane of thyroid follicular cells. Although pendrin was shown to transport iodide and chloride using Xenopus laevis oocytes and Sf9 insect cells, there is no report using mammalian cells to study its role in thyroid function. We show here, using COS-7 cells and Chinese hamster ovary cells transfected with expression vectors encoding sodium iodide symporter or human Pendred syndrome gene cDNA and by comparison with studies using rat thyroid FRTL-5 cells, that pendrin is an iodide-specific transporter in mammalian cells and is responsible for iodide efflux in the thyroid.

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