title: Iodide excess regulates its own efflux: a possible involvement of pendrin.
abstract: Adequate iodide supply and metabolism are essential for thyroid hormones synthesis. In thyrocytes, iodide uptake is mediated by the sodium-iodide symporter, but several proteins appear to be involved in iodide efflux. Previous studies demonstrated that pendrin is able to mediate apical efflux of iodide in thyrocytes. Acute iodide excess transiently impairs thyroid hormone synthesis, a phenomenon known as the Wolff-Chaikoff effect. Although the escape from this inhibitory effect is not completely understood, it has been related to the inhibition of sodium-iodide symporter-mediated iodide uptake. However, the effects of iodide excess on iodide efflux have not been characterized. Herein, we investigated the consequences of iodide excess on pendrin abundance, subcellular localization, and iodide efflux in rat thyroid PCCl3 cells. Our results indicate that iodide excess increases pendrin abundance and plasma membrane insertion after 24 h of treatment. Moreover, iodide excess increases pendrin half-life. Finally, iodide exposure also increases iodide efflux from PCCl3 cells. In conclusion, these data suggest that pendrin may have an important role in mediating iodide efflux in thyrocytes, especially under conditions of iodide excess.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil; and.
authors.forename: Jamile
authors.initials: J
authors.lastname: Calil-Silveira
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil; and.
authors.forename: Caroline
authors.initials: C
authors.lastname: Serrano-Nascimento
authors.affiliation: Division of Endocrinology Metabolism and Molecular Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
authors.forename: Peter Andreas
authors.initials: PA
authors.lastname: Kopp
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil; and mtnunes@icb.usp.br.
authors.forename: Maria Tereza
authors.initials: MT
authors.lastname: Nunes
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D027963:Chloride-Bicarbonate Antiporters / Q000378:metabolism*; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D051381:Rats; D060888:Real-Time Polymerase Chain Reaction; D012974:Sodium Iodide / Q000378:metabolism* / Q000494:pharmacology*; D000076988:Sulfate Transporters; D060168:Thymocytes / Q000187:drug effects* / Q000378:metabolism
chemical_list: D027963:Chloride-Bicarbonate Antiporters; C494615:Slc26A4 protein, rat; D000076988:Sulfate Transporters; D012974:Sodium Iodide
keywords: Wolff-Chaikoff effect escape; iodide efflux; iodide excess; pendrin