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

• Published in: Biochemical and biophysical research communications Vol. 426; no. 4; pp. 615 - 619
• Main Authors: Li, Yangxin, Shelat, Harnath, Geng, Yong-Jian
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 05-10-2012
• Subjects: 3' Untranslated Regions - genetics; Apoptosis; Cells, Cultured; Cytochrome-c; Cytochromes c - metabolism; Humans; Hydrogen Peroxide - pharmacology; IGF-1; Induced Pluripotent Stem Cells - drug effects; Induced Pluripotent Stem Cells - metabolism; Induced Pluripotent Stem Cells - physiology; Insulin-Like Growth Factor I - genetics; Insulin-Like Growth Factor I - physiology; iPS cells; microRNA; MicroRNAs - genetics; MicroRNAs - metabolism; Mitochondria; Mitochondria - metabolism; Mitochondrial Diseases - metabolism; Oxidative Stress; microRNA; Mitochondria; IGF-1; iPS cells; Apoptosis; Cytochrome-c
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2012.08.139

► 3′-Untranslated regions of IGF-1 gene is a target of miR-1 in iPS cells. ► H2O2 increases miR-1 expression in iPS cells. ► IGF-1 prevents apoptosis of iPS cells. ► miR-1 mimic blocks the protective effects of IGF-1 on H2O2-induced cytotoxicity. ► miR-1 mimic control did not attenuate the effects of IGF-1 in iPS cells.
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.