c-erb-A mRNA Correlates with T₃-Receptor Levels in Liver and Pituitary of Tumor Rats

Abstract

In the rat tumor model of the sick euthyroid syndrome, differential regulation of T3-induced cellular responses have been demonstrated in liver and anterior pituitary. These effects occur with a concomitant decrease in nuclear thyroid hormone receptor (TR) number as measured by the binding of 125I-labeled T3. To explore the possibility that these altered responses to T3 in tumor rats resulted from changes in the expression of different TR forms, we correlated the relative abundance of mRNAs encoding each receptor form with the concentration of TR measured by specific T3 binding. In anterior pituitary of tumor rats, TR beta-1 and beta-2 mRNA levels decreased to 51 and 45%, respectively, compared to controls; rat c-erb A alpha-2 mRNA, which encodes a TR-related DNA alpha-binding protein that does not bind T3, decreased to 46% of control. These findings correlate with a decrease in nuclear T3 binding capacity that has been shown to be 63% of control. The level of TR beta-1 mRNA, the only quantifiable TR form in liver, was decreased to 61% of control in the same hepatic tissue that revealed a 50% decrease in TR as measured by specific T3 binding. The coordinate down-regulation of all TR mRNA forms to a degree that parallels the decrease in TR number as measured by specific T3 binding suggests that the differential regulation of T3-mediated effects in illness is by a mechanism other than changing concentrations of specific receptor forms.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential Modulation of Liver and Pituitary Triiodothyronine and 9-cisRetinoid Acid Receptors by Insulin-Like Growth Factor I in Rats

“…It seems to be the case of the results obtained in this study where a concurrent reduction of liver and pituitary TR mRNAs and TR proteins induced by IGF-I administration to rats was observed. A similar correlation between TR mRNA and TR protein levels in liver and pituitary of tumor rats has also been reported (48). Furthermore, we investigated the possible transcriptional mechanism of TR gene regulation by IGF-I in liver.…”

Thyroid hormone receptor β1 gene expression is increased by Dexamethasone at transcriptional level in rat liver

“…However, physiological or pharmacological factors may also induce transcriptional and posttranscriptional modifications in the mRNA abundance that parallel the level of its protein (Huppart et al, 1993). This seems to be the case of the results obtained on the effect exerted by Dex, although the increase of TRh 1 mRNA was detected by lower doses of Dex than TRh 1 protein.…”