Key result
Histone H3 methylation is altered in failing cardiomyocytes, with K4TM showing greater disease-related changes than K9TM.
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Epigenetic alterations are implicated in the development of cardiac hypertrophy and heart failure, but little is known of which epigenetic changes in which regions of the genome play such a role. We now show that trimethylation of histone H3 on lysine-4 (K4TM) or lysine-9 (K9TM) is markedly affected in cardiomyocytes in association with the development of heart failure in a rat disease model. High-throughput pyrosequencing performed with ChIP products for K4TM or K9TM prepared from human left ventricular tissue with retained or damaged function also revealed that protein-coding genes located in the vicinity of K4TM marks differ between functional and disabled myocytes, yet both sets of genes encode proteins that function in the same signal transduction pathways for cardiac function, indicative of differential K4TM marking during the development of heart failure. However, K9TM mark-profile was less dependent on the disease status compared to that of K4TM. Our data collectively reveal global epigenetic changes in cardiac myocytes associated with heart failure.
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Kaneda et al. (2008) studied Heart failure. Histone H3 trimethylation on lysine-4 (K4TM) and lysine-9 (K9TM) vs. Functional myocytes / retained left ventricular function was evaluated on Genome-wide histone methylation profile (K4TM and K9TM marks) near protein-coding genes. Trimethylation of histone H3 on lysine-4 (K4TM) and lysine-9 (K9TM) was markedly altered in failing cardiomyocytes, with K4TM marks differing more by disease status than K9TM.
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