Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

Thyroid dysfunction is classified into hyperthyroidism and congenital hypothyroidism (CH). Both hyperthyroidism and CH can cause heart lesions; however, the mechanisms involved remain unclear. The left ventricle was collected from eu-, hyper-, and hypothyroid rat. RNA was extracted and reverse-transcripted to cDNA. Real-time fluorescence quantitation-PCR was used to quantify the differential expression of thyroid hormone receptor (TR) subtype mRNA among eu-, hyper-, and hypothyroid rat myocardium. Here, we show that compared with the normal myocardium, TRalpha1 mRNA expression was upregulated by 51% (P<0.01), TRalpha2 mRNA expression was downregulated by 58% (P<0.01), and TRbeta1 mRNA expression remained unchanged in hyperthyroid rat myocardium (P>0.05). TRalpha1, TRalpha2, and TRbeta1 were expressed in normal and hypothyroid rat myocardium throughout the developmental process. In hypothyroid rats, myocardial TRalpha1 mRNA expression was generally downregulated and the expression peak appeared late. Myocardial TRalpha2 mRNA expression was generally upregulated and the expression peak appeared late. Myocardial TRbeta1 mRNA expression was generally downregulated and changed similarly with the control group. In addition, the hypogenetic myocardium can be seen in the hypothyroid rat by pathology study. Taken together, the abnormal expression of TR subtype mRNA may have a close relationship with the pathogenesis of CH and hyperthyroidism heart disease.