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Post-transcriptional induction of β₁-adrenergic receptor by retinoic acid, but not triiodothyronine, in C6 glioma cells expressing thyroid hormone receptors

López-Barahona M, Iglesias T, García-Higuera I, Mayor Jr F, Zaballos A, Bernal J, Muñoz A. Posttranscriptional induction of β₁ -adrenergic receptor by retinoic acid, but not triiodothyronine, in C6 glioma cells expressing thyroid hormone receptors. Eur J Endocrinol 1996:135:709–15. ISSN 0804–4643

Thyroid hormone (triiodothyronine; T₃) has been shown to control the expression of β₁ -adrenergic receptors (β₁-AR) in cardiac myocytes, but not in C6 glioma cells. This cell specificity has been attributed to low expression of T₃ receptors and high expression of the c-erbA₂ splice variant that interferes with the action of T₃. To check this hypothesis we have expressed the c-erbA/thyroid hormone receptor (TR) ₁ gene in C6 glioma cells and investigated their response to thyroid hormone. Cells expressing TR₁, but not wild-type cells, were responsive to T₃ as shown by increased expression of mitochrondrial hydroxymethylglutaryl CoA synthase after T₃ exposure. However, T₃ had no effect on β₁-AR gene expression in either set of cells. The β₁-AR mRNA concentrations were, however, altered by retinoic acid (RA) treatment. Retinoic acid caused a rapid up-regulation of β₁-AR mRNA levels that was blocked by cycloheximide. Retinoic acid did not increase the β₁-AR gene transcription rate in run-on experiments. These results indicate an indirect post-transcriptional effect of RA. Control of β₁-AR expression in C6 cells is also exerted at the translational level, because there was no correlation between mRNA and protein induction, as determined by radioligand binding studies. We conclude that lack of responsiveness of the β₁-AR gene in C6 cells to T₃ is not due to high expression of c-erbA₂ but to undefined cell-specific factors.

Alberto Muñoz, Instituto Investigaciones Biomedicas, Arturo Duperier 4, 28029 Madrid, Spain