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Selenium increases thyrotrophin-induced NIS expression through Ape1-dependent regulation of Pax8 binding activity

AutorLeoni, Suzana G.; Sastre-Perona, Ana ; Santisteban, Pilar ; Vieja, Antonio de la
Fecha de publicación2014
CitaciónETA 2014
ResumenThe sodium iodide symporter (NIS) mediates the uptake of I- by the thyroid follicular cell being the first step of hormones biosynthesis. NIS function is stimulated by TSH and requires PAX8 binding within NUE (Nis upstream enhancer). In this study we investigate the role of selenium on Nis expression through the regulation of Pax8 DNA-binding activity. [Results]: Selenium (Se) treatment increased TSH-induced Nis mRNA and protein expressions, as well as Nis activity, in the PCCl3 thyroid cells. We considered that Pax8 could be involved in this effect, since Se stimulus was only observed for Nis promoter containing NUE. In fact, Se increased Pax8 expression and its DNA-binding activity. Also, in null-Pax8 PCCl3 cell Nis is not Se responsive, confirming the crucial role of Pax8 in these responses. Two antioxidant enzymes were considered as putative mediators of this mechanism: TxnRd1 and Ape1. First we inhibited TxnRd1 activity by auranofin and no alteration was observed on Se stimulus. However when Ape1 was inhibited by E3330 both, TSH or TSH/Se stimulus, was no longer observed. Ape1 proved to be essential both for Pax8 binding activity as well as for Nis expression. [Conclusion]: Under basal oxidation levels, Nis expression is controlled by Ape1 through a TSH/Se-dependent mechanism. These findings open a new field about the importance of Se in the thyroid physiology.
DescripciónResumen del trabajo presentado al 38th Annual Meeting of the European Thyroid Association celebrado en Santiago de Compostela (España) del 6 al 10 de septiembre de 2014.
URIhttp://hdl.handle.net/10261/125609
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