Abstract
IntroductionThe expression of hundreds of genes is altered in response to left ventricular (LV) remodeling following large transmural myocardial infarction (MI). Thyroid hormone (TH) improves LV remodeling and cardiac performance after MI. However, the molecular basis is unknown.MethodsMI was produced by ligation of the left anterior descending coronary artery in female SD rats. Rats were divided into the following groups: (1) Sham MI, (2) MI, and (3) MI+T4 treatment (T4 pellet 3.3 mg, 60 days release, implanted subcutaneously immediately following MI). Four weeks after surgery, total RNA was isolated from LV non-infarcted areas for microarray analysis using the Illumina RatRef-12 Expression BeadChip Platform.ResultsSignals were detected in 13,188 genes (out of 22,523), of which the expression of 154 genes were decreased and the expression of 200 genes were increased in MI rats compared with Sham MI rats (false discovery rate (FDR) <0.05). Compared to MI rats, T4 treatment decreased expression of 27 genes and increased expression of 28 genes. In particular, 6 genes down-regulated by MI and 12 genes up-regulated by MI were reversed by T4. Most of the 55 genes altered by T4 treatment are in the category of molecular function under binding (24) and biological processes which includes immune system process (9), multi-organism process (5) and biological regulation (19) nonexclusively.ConclusionsThese results suggest that altered expression of genes for molecular function and biological process may be involved in the beneficial effects of thyroid hormone treatment following MI in rats.
Highlights
The expression of hundreds of genes is altered in response to left ventricular (LV) remodeling following large transmural myocardial infarction (MI)
Results showed that thyroid hormone can reduce myocyte apoptosis and improve left ventricular remodeling and LV function after MI [3,4,5,6,7,8]
No difference was found in infarct area between MI and MI+T4 groups (Table 1), three animals in each of MI and MI+T4 groups with infarct area,30% were excluded from this study
Summary
The expression of hundreds of genes is altered in response to left ventricular (LV) remodeling following large transmural myocardial infarction (MI). Thyroid hormone (TH) improves LV remodeling and cardiac performance after MI. Left ventricular (LV) remodeling is a complicated process following a large transmural myocardial infarction (MI) involving both infarct and non-infarcted regions with changes in myocytes, interstitial matrix, and vasculature [1]. Targeted treatments that improve this process, such as b-blockers and angiotensin converting enzyme inhibitors, have led to great progress in alleviation of heart failure in post-MI patients. Results showed that thyroid hormone can reduce myocyte apoptosis and improve left ventricular remodeling and LV function after MI [3,4,5,6,7,8]. Thyroid hormone receptors and some signal pathways have been proposed to mediate these effects, the underlying gene changes are still not clear
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