NDLI: Insulin ameliorates miR-1-induced injury in H9c2 cells under oxidative stress via Akt activation

Content Provider	Springer Nature Link
Author	Chen, Tao Ding, Guoliang Jin, Zhuqing Wagner, Mary B. Yuan, Zuyi
Copyright Year	2012
Abstract	Growing evidence indicates that aberrant upregulation of microRNA-1 (miR-1) occurs in ischemic myocardium. In addition, insulin elicits metabolism-independent cardioprotection against cardiovascular diseases. The aim of this study is to determine whether insulin ameliorates miR-1-induced injury in H9c2 cells under oxidative stress and to investigate the underlying mechanisms. By quantitative real-time RT-PCR (qRT-PCR), we show that miR-1 is upregulated in H9c2 cells after treatment with hydrogen peroxide (H$_{2}$O$_{2}$), and this effect is both dose- and time dependent. Furthermore, expression of miR-1 decreased significantly after insulin treatment (4.5 ± 0.1 vs. 3.0 ± 0.2, p < 0.05). To determine the potential role of miR-1 in cellular injury and gene regulation, adenovirus-mediated overexpression of miR-1 was used. Overexpression of miR-1 decreased cell viability by 28 ± 2 % (n = 6, p < 0.05) and damaged Akt activation with or without H$_{2}$O$_{2}$ treatment. To further investigate the effect of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in miR-1-induced injury, H9c2 cells were pretreated with LY294002 (10 μM LY, a specific inhibitor of PI3K) with or without insulin (100 nM) and subjected to H$_{2}$O$_{2}$ treatment. LY pretreatment-inhibited Akt activation, lead to increased reactive oxygen species (ROS), and further decreased cell viability induced by miR-1 (n = 6, p < 0.05, n = 9–10 cells/group, p < 0.05 and n = 6, p < 0.05) under oxidative stress. This effect was abolished by insulin. In summary, our findings suggest that miR-1expression is sensitive to H$_{2}$O$_{2}$ stimulation. In addition, insulin decreases miR-1 expression and induces a marked protective effect on miR-1-induced injury under oxidative stress, which may be mediated by the Akt-mediated pathway. These results provide an important, novel clue as to the mechanism of the cardiovascular action of insulin.
Starting Page	167
Ending Page	174
Page Count	8
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	369
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2012-07-18
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	H9c2 cardiomyoblast Oxidative stress microRNA-1 Insulin Akt Cardiology Oncology Medical Biochemistry Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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