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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Upregulation of thyroid hormone receptor beta 1 and beta 2 messenger RNA in the myocardium of dogs with dilated cardiomyopathy or chronic valvular disease.

OBJECTIVE: To investigate whether expression of thyroid hormone receptor ( TR) messenger RNA (mRNA) is changed in the myocardium of dogs with heart failure. ANIMALS: 21 dogs. PROCEDURE: Concentrations of TR alpha 2, beta 1, and beta 2 mRNA in the myocardium were determined for clinically normal dogs (n = 7) and dogs with heart failure caused by dilated cardiomyopathy (DCM; 7) or chronic valvular disease (CVD; 7). Concentrations were quantified by use of reverse transcription-polymerase chain reaction and ELISA. RESULTS: The ratio of expression of TR alpha 2, beta 1, and beta 2 mRNA was typically 100:10:1. Differences in concentration of TR alpha 2 mRNA among the 3 groups of dogs were not detected, but concentrations of TR beta 1 and beta 2 mRNA were greater in diseased myocardium. Thyroid hormone receptor beta 1 mRNA was upregulated approximately threefold, and TR beta 2 mRNA was upregulated approximately eightfold in myocardium of dogs with DCM and CVD, compared with clinically normal dogs. There was no difference in TR beta 1 and beta 2 mRNA upregulation between dogs with DCM and CVD. CONCLUSIONS AND CLINICAL RELEVANCE: Altered regulation of transcription of the TR beta gene may be one facet of the myocardial phenotype in heart failure. Because this phenotypic response did not differ on the basis of cause (DCM vs CVD), it appears to be a secondary effect of heart failure and the alteration in metabolism of thyroid hormone. Treatment of dogs with heart failure with thyroid hormone or thyroid hormone analogues may improve cardiac performance.[1]


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