Thyroid hormone receptor beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver

MONTESINOS, MM; PELLIZAS, CG; VÉLEZ ML; SUSPERREGUY S; MASINI-REPISO AM; COLEONI AH

Pergamon Press

Lugar: Oxford; Año: 2006 vol. 78 p. 2584 - 2584

riiodothyronine (T3) exerts most of its effect through nuclear thyroid hormone receptors (TR) which bind mainly as heterodimers with retinoid-X receptors (RXR) to thyroid hormone response elements (TRE) in target genes. It is well known the synergistic interaction of T3 and glucocorticoids on the synthesis of growth hormone in rat pituitary cell lines and in the T3-induced metamorphosis in amphibians. Glucocorticoids increased mRNAs of T3-regulated hepatic genes. Our laboratory reported increased specific metabolic actions of T3 in rat liver by Dexamethasone (Dex) through a mechanism involving an up-regulation of the maximal binding capacity of TR. In this study we further explored the participation of TR in the molecular mechanism of the Dex-induced increase on liver T3 metabolic action. Dex administration to adrenalectomized rats induced an increase of liver TR beta protein and mRNA. Nuclear run-on assay revealed that Dex up-regulated the TR gene transcriptional rate. Transfection a