Genome-wide histone methylation profile for heart failure

被引：118

作者：

Kaneda, Ruri ^{[1
,2
]}

Takada, Shuji ^{[1
]}

Yamashita, Yoshihiro ^{[1
]}

Choi, Young Lim ^{[1
]}

Nonaka-Sarukawa, Mutsuko ^{[2
]}

Soda, Manabu ^{[1
]}

Misawa, Yoshio ^{[3
]}

Isomura, Tadashi ^{[4
]}

Shimada, Kazuyuki ^{[2
]}

Mano, Hiroyuki ^{[1
,5
]}

机构：

[1] Jichi Med Univ, Div Funct Genom, Mibu, Tochigi 3290498, Japan

[2] Jichi Med Univ, Div Cardiovasc Med, Mibu, Tochigi 3290498, Japan

[3] Jichi Med Univ, Div Cardiovasc Surg, Mibu, Tochigi 3290498, Japan

[4] Hayama Heart Ctr, Kanagawa 2400116, Japan

[5] Japan Sci & Technol Agcy, CREST, Kawaguchi, Saitama 3320012, Japan

来源：

GENES TO CELLS | 2009年 / 14卷 / 01期

关键词：

CARDIAC-HYPERTROPHY; MICROARRAY ANALYSIS; GENE-EXPRESSION; CANCER-CELLS; CHROMATIN; RECRUITMENT; STRESS; MOUSE;

D O I：

10.1111/j.1365-2443.2008.01252.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：69 / 77

页数：9

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