MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes

被引：180

作者：

Horie, Takahiro

Ono, Koh ^{[1
]}

Nishi, Hitoo

Iwanaga, Yoshitaka ^{[2
]}

Nagao, Kazuya

Kinoshita, Minako

Kuwabara, Yasuhide

Takanabe, Rieko ^{[3
]}

Hasegawa, Koji ^{[3
]}

Kita, Toru

Kimura, Takeshi

机构：

[1] Kyoto Univ, Dept Cardiovasc Med, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

[2] Kinki Univ, Dept Cardiovasc Med, Grad Sch Med, Osakasayama, Japan

[3] Natl Hosp Org, Div Translat Res, Kyoto Med Ctr, Kyoto, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 389卷 / 02期

关键词：

MicroRNA; GLUT4; Cardiomyocyte; CHRONIC HEART-FAILURE; INSULIN-RESISTANCE; GLUCOSE TRANSPORTERS; GENE-EXPRESSION; TRANSGENIC MICE; ADIPOSE-TISSUE; HYPERTROPHY; DISEASE; RATS; DIFFERENTIATION;

D O I：

10.1016/j.bbrc.2009.08.136

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

GLUT4 shows decreased levels in failing human adult hearts. We speculated that GLUT4 expression in cardiac muscle may be fine-tuned by microRNAs. Forced expression of miR-133 decreased GLUT4 expression and reduced insulin-mediated glucose uptake in cardiomyocytes. A computational miRNA target prediction algorithm showed that KLF15 is one of the targets of miR-133. It was confirmed that overexpression of miR-133 reduced the protein level of KLF15, which reduced the level of the downstream target GLUT4. Cardiac myocytes infected with lenti-decoy, in which the 3'UTR with tandem sequences complementary to miR-133 was linked to the luciferase reporter gene, had decreased miR-133 levels and increased levels of GLUT4. The expression levels of KLF15 and GLUT4 were decreased at the left ventricular hypertrophy and congestive heart failure stage in a rat model. The present results indicated that miR-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiomyocytes. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：315 / 320

页数：6

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