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 μg/100 g BW, i...

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Published in:Molecular and cellular endocrinology Vol. 226; no. 1; pp. 19 - 26
Main Authors: Giannocco, Gisele, DosSantos, Rosangela A., Nunes, Maria Tereza
Format: Journal Article
Language:English
Published: Ireland Elsevier Ireland Ltd 29-10-2004
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Summary: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 μg/100 g BW, i.p., 5 days) and time-course studies (100 μg/100 g BW, i.v., from 0.5 to 24 h), 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 μg/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.
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ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2004.07.007