Minireview: The sodium-iodide symporter NIS and pendrin in iodide homeostasis of the thyroid.

Détails

ID Serval
serval:BIB_0ECA436B5712
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Minireview: The sodium-iodide symporter NIS and pendrin in iodide homeostasis of the thyroid.
Périodique
Endocrinology
Auteur⸱e⸱s
Bizhanova A., Kopp P.
ISSN
1945-7170 (Electronic)
ISSN-L
0013-7227
Statut éditorial
Publié
Date de publication
03/2009
Peer-reviewed
Oui
Volume
150
Numéro
3
Pages
1084-1090
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Review
Publication Status: ppublish
Résumé
Thyroid hormones are essential for normal development and metabolism. Thyroid hormone biosynthesis requires iodide uptake into the thyrocytes and efflux into the follicular lumen, where it is organified on selected tyrosyls of thyroglobulin. Uptake of iodide into the thyrocytes is mediated by an intrinsic membrane glycoprotein, the sodium-iodide symporter (NIS), which actively cotransports two sodium cations per each iodide anion. NIS-mediated transport of iodide is driven by the electrochemical sodium gradient generated by the Na(+)/K(+)-ATPase. NIS is expressed in the thyroid, the salivary glands, gastric mucosa, and the lactating mammary gland. TSH and iodide regulate iodide accumulation by modulating NIS activity via transcriptional and posttranscriptional mechanisms. Biallelic mutations in the NIS gene lead to a congenital iodide transport defect, an autosomal recessive condition characterized by hypothyroidism, goiter, low thyroid iodide uptake, and a low saliva/plasma iodide ratio. Pendrin is an anion transporter that is predominantly expressed in the inner ear, the thyroid, and the kidney. Biallelic mutations in the SLC26A4 gene lead to Pendred syndrome, an autosomal recessive disorder characterized by sensorineural deafness, goiter, and impaired iodide organification. In thyroid follicular cells, pendrin is expressed at the apical membrane. Functional in vitro data and the impaired iodide organification observed in patients with Pendred syndrome support a role of pendrin as an apical iodide transporter.
Mots-clé
Animals, Gene Expression Regulation, Homeostasis/physiology, Humans, Iodine/metabolism, Membrane Transport Proteins/metabolism, Membrane Transport Proteins/physiology, Metabolism, Inborn Errors/etiology, Metabolism, Inborn Errors/genetics, Metabolism, Inborn Errors/metabolism, Models, Biological, Sulfate Transporters, Symporters/genetics, Symporters/metabolism, Symporters/physiology, Syndrome, Thyroid Gland/metabolism, Thyroid Gland/physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
30/12/2020 13:56
Dernière modification de la notice
31/12/2020 6:26
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