ArticleMolecular and cellular biochemistry2012
Insulin ameliorates miR-1-induced injury in H9c2 cells under oxidative stress via Akt activation.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 38 citations in OpenAlex.
- Reactive oxygen species in fetal growth restriction mechanisms and therapeutic directions (Review).International journal of molecular medicine · 2026Review
- Identification of Connexin 26 on Extracellular Vesicles from Human Cardiomyocytes and Plasma: Novel Insights into miRNA Loading and Oxidative Injury.International journal of molecular sciences · 2025Article
- Roxadustat improves diabetic myocardial injury by upregulating HIF-1α/UCP2 against oxidative stress.Cardiovascular diabetology · 2025Article
- Identification of miR-1 and miR-499 in chronic atrial fibrillation by bioinformatics analysis and experimental validation.Frontiers in cardiovascular medicine · 2024Article
- Identification of Novel Insulin Resistance Related ceRNA Network in T2DM and Its Potential Editing by CRISPR/Cas9.International journal of molecular sciences · 2021Article
- Circular RNAs: Novel Players in the Oxidative Stress-Mediated Pathologies, Biomarkers, and Therapeutic Targets.Oxidative medicine and cellular longevity · 2021Review
- Soluble Epoxide Hydrolase Inhibitors Regulate Ischemic Arrhythmia by Targeting MicroRNA-1.Frontiers in physiology · 2021Article
- miR-27b Modulates Insulin Signaling in Hepatocytes by Regulating Insulin Receptor Expression.International journal of molecular sciences · 2020Article
- Potential Clinical Implications of miR-1 and miR-21 in Heart Disease and Cardioprotection.International journal of molecular sciences · 2020Review
- Incremental effect of liraglutide on traditional insulin injections in rats with type 2 diabetes mellitus by maintaining glycolipid metabolism and cardiovascular function.Experimental and therapeutic medicine · 2019Article
- The Destiny of Glucose from a MicroRNA Perspective.Frontiers in endocrinology · 2018Review
- Paeoniflorin inhibits doxorubicin-induced cardiomyocyte apoptosis by downregulating microRNA-1 expression.Experimental and therapeutic medicine · 2016Article
- Article
- MicroRNAs in congenital heart disease.Annals of translational medicine · 2015Review
- MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network.Cell stress & chaperones · 2015Article
- miR-133a enhances the protective capacity of cardiac progenitors cells after myocardial infarction.Stem cell reports · 2014Article
- Looking into a conceptual framework of ROS-miRNA-atrial fibrillation.International journal of molecular sciences · 2014Review
- PI3K/Akt/uncoupling protein 2 signaling pathway may be involved in cell senescence and apoptosis induced by angiotensin II in human vascular endothelial cells.Molecular biology reports · 2014Article
- Involvement of miRNAs in placental alterations mediated by oxidative stress.Oxidative medicine and cellular longevity · 2014Review
- Acute hyperglycemia abolishes ischemic preconditioning by inhibiting Akt phosphorylation: normalizing blood glucose before ischemia restores ischemic preconditioning.Oxidative medicine and cellular longevity · 2013Article
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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-1 expression 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.
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