IGF-1 prevents oxidative stress induced-apoptosis in induced pluripotent stem cells which is mediated by microRNA-1

被引:48
作者
Li, Yangxin [1 ]
Shelat, Harnath
Geng, Yong-Jian [2 ]
机构
[1] Univ Texas Med Sch, Texas Heart Inst, Houston, TX 77030 USA
[2] Univ Texas Med Sch, Ctr Cardiovasc & Atherosclerosis Res, Dept Internal Med, Houston, TX 77030 USA
基金
美国国家卫生研究院;
关键词
iPS cells; IGF-1; microRNA; Apoptosis; Cytochrome-c; Mitochondria; CYTOCHROME-C RELEASE; INDUCED MITOCHONDRIAL DYSFUNCTION; HEART; ACTIVATION; ACID; CARDIOMYOCYTES; CASPASE-9; PATTERN;
D O I
10.1016/j.bbrc.2012.08.139
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Oxidative stress contributes to tissue injury and cell death during the development of various diseases. The present study aims at investigating whether oxidative stress triggered by the exposure to hydrogen peroxide (H2O2) can induce apoptosis of induced pluripotent stem cells (iPS cells) in a mechanism mediated by insulin-like growth factor (IGF-1) and microRNA-1 (miR-1). iPS cells treated with H2O2 showed increases in miR-1 expression, mitochondria dysfunction, cytochrome-c release and apoptosis, Addition of IGF-1 into the iPS cell cultures reduced the H2O2 cytotoxicity. Prediction algorithms showed that 3'-untranslated regions of IGF-1 gene as a target of miR-1. Moreover, miR-1 mimic, but not miR-1 mimic negative control, diminished the protective effect of IGF-1 on H2O2-induced mitochondrial dysfunction, cytochrome-c release and apoptosis in iPS cells. In conclusion, IGF-1 inhibits H2O2-induced mitochondrial dysfunction, cytochrome-c release and apoptosis. IGF-1's effect is, at least partially, regulated by miR-1 in iPS cells. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:615 / 619
页数:5
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