Thyroid hormones (THs) enhance MHC α gene- and repress MHC β gene-transcription in the heart, by interacting with specific nuclear receptors (TRs), that bind to regulatory sequences localized upstream of basal promoter of myosin heavy chain (MHC) genes. The overall effects of THs include an increase in V1- and a decrease in V3-myosin isozyme concentration in the heart. Myosin V1 contains two MHC α chains and has a higher ATPase activity than V3 isoform, which contains two β chains. Previous studies on papillary muscles of spontaneously hypertensive rats (SHRs) showed that heart hypertrophy is accompanied by a shift from α to β MHC accumulation. The present study was aimed at evaluating whether this event relates to differential expression of α1, α2, and β1 isoforms of TRs. At the ages of 8 and 15 weeks, SHRs and Harlan Sprague-Dawley control rats were sacrificed under anesthesia and their hearts were dissected into left and right ventricles, free of atria and great vessels. The results of Western blot analyses showed that the levels of the three TR isoforms do not differ significantly between SHRs and control rats of the same age, either in the left or in the right ventricle. Thus, the expression of MHC β in SHR hypertrophic heart does not seem to depend on changes in TR isoform concentrations.

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