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Genome‐wide histone methylation profile for heart failure
Author(s) -
Kaneda Ruri,
Takada Shuji,
Yamashita Yoshihiro,
Choi Young Lim,
akaSarukawa Mutsuko,
Soda Manabu,
Misawa Yoshio,
Isomura Tadashi,
Shimada Kazuyuki,
Mano Hiroyuki
Publication year - 2009
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2008.01252.x
Subject(s) - biology , epigenetics , histone , heart failure , gene , myocyte , genetics , dna methylation , methylation , microbiology and biotechnology , bioinformatics , gene expression , medicine
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.