Upregulation of thyroid hormone receptor beta(1) and beta(2) messenger RNAin the myocardium of dogs with dilated cardiomyopathy or chronic valvular disease

Citation
S. Shahrara et al., Upregulation of thyroid hormone receptor beta(1) and beta(2) messenger RNAin the myocardium of dogs with dilated cardiomyopathy or chronic valvular disease, AM J VET RE, 60(7), 1999, pp. 848-852
Citations number
44
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
AMERICAN JOURNAL OF VETERINARY RESEARCH
ISSN journal
00029645 → ACNP
Volume
60
Issue
7
Year of publication
1999
Pages
848 - 852
Database
ISI
SICI code
0002-9645(199907)60:7<848:UOTHRB>2.0.ZU;2-#
Abstract
Objective-To investigate whether expression of thyroid hormone receptor (TR ) messenger RNA (mRNA) is changed in the myocardium of dogs with heart fail ure. 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 c hronic 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 wa s typically 100:10:1. Differences in concentration of TR alpha(2) mRNA amon g 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 recep tor beta(1) mRNA was upregulated approximately threefold, and TR beta(2) mR NA was upregulated approximately eightfold in myocardium of dogs with DCM a nd 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 t he TR beta gene may be one facet of the myocardial phenotype in heart failu re. 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 a lteration in metabolism of thyroid hormone. Treatment of dogs with heart fa ilure with thyroid hormone or thyroid hormone analogues may improve cardiac performance.