Thyroid hormone stimulates myoglobin gene expression in rat cardiac muscle

T-3 increases the heart activity, O-2 consumption and the reactive O-2 species production. Myoglobin (Mb) is highly expressed in the heart, where it facilitates O-2 diffusion, mitochondrial respiration, and scavenges reactive O-2 species. Here we investigate, by dose-response (0.3-100 mug/100g BW, i.p., 5 days) and time-course studies (100 mug/100 g BW, i.v., from 0.5 to 24h), whether T-3 affects the Mb mRNA and protein expression in atrium (A) and ventricle (V), by Northern and Western blot. We show that the Mb gene is controlled by T-3 in A and V, as indicated by Mb mRNA and protein content decrease in thyroidectomized (Tx) rats, and restoration by T-3 treatment. In the A, the different doses of T-3 induced the Mb mRNA and protein recovery to the euthyroid levels; in the time-course study, this occurred only with the protein levels. In the V, T-3 progressively increased the Mb mRNA above the euthyroid levels at a dose of 25 mug/100 g BW; higher doses decreased it to the euthyroid levels. Mb protein increased only to the euthyroid levels at all T-3 doses injected. The time-course study showed a progressive increase in the ventricular Mb mRNA and protein, which exceeded the euthyroid levels from 6 to 24 h, and at 2 and 6 h of the T-3 treatment, respectively. We conclude that heart Mb gene expression is influenced by thyroid status. (C) 2004 Elsevier Ireland Ltd. All rights reserved.