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The effect of tri-iodothyronine (T₃) treatment on myocardial levels of and β myosin heavy chain (MHC) mRNAs in the rat was defined in vivo and in vitro. Dose–response experiments were performed in intact hypothyroid and euthyroid rats; in addition, studies in vitro examined the effect of T₃ on MHC mRNAs in neonatal cardiac myocytes in primary culture. Specific and β MHC mRNAs were determined by Northern blot and dot hybridization to oligonucleotide probes complementary to the 3' untranslated regions of the MHC genes. An increase in myocardial β MHC mRNA was demonstrated in hypothyroidism, accompanied by a reduction in MHC mRNA. Marked differences in the sensitivity of and β MHC mRNAs to T₃ replacement were found; a dose-dependent increase in mRNA was evident at 6 h after T₃ treatment, in the absence of consistent effects on β mRNA, whereas 72 h after T₃ replacement was commenced, stimulatory effects of T₃ on MHC mRNA, evident at all doses, were accompanied by a dose-dependent inhibition of β MHC mRNA. No effect of thyroid status on actin mRNA was found, indicating the specificity of MHC gene regulation. T₃ treatment of cardiac myocytes in vitro exerted similar actions on MHC mRNAs to those found in vivo, with a more marked influence on than β MHC mRNA. These studies of the action of T₃ in vivo and in vitro have thus demonstrated specific effects of T₃ on pretranslational regulation of the and β MHC genes, influences which differ not only in terms of stimulation or inhibition, but also in magnitude of effect.

Journal of Endocrinology (1989) 122, 193–200

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