Thyroid hormone stimulates myoglobin gene expression in rat cardiac muscle.

T3 increases the heart activity, O2 consumption and the reactive O2 species production. Myoglobin (Mb) is highly expressed in the heart, where it facilitates O2 diffusion, mitochondrial respiration, and scavenges reactive O2 species. Here we investigate, by dose-response (0.3-100 microg/100 g BW, i.p., 5 days) and time-course studies (100 microg/100 g BW, i.v., from 0.5 to 24h), whether T3 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 T3 in A and V, as indicated by Mb mRNA and protein content decrease in thyroidectomized (Tx) rats, and restoration by T3 treatment. In the A, the different doses of T3 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, T3 progressively increased the Mb mRNA above the euthyroid levels at a dose of 25 microg/100g BW; higher doses decreased it to the euthyroid levels. Mb protein increased only to the euthyroid levels at all T3 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 24h, and at 2 and 6 h of the T3 treatment, respectively. We conclude that heart Mb gene expression is influenced by thyroid status.