ArticlePloS one2015
MicroRNAs Regulate Cellular ATP Levels by Targeting Mitochondrial Energy Metabolism Genes during C2C12 Myoblast Differentiation.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 53 citations in OpenAlex.
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- Effects of hypoxia and reoxygenation on mitochondrial functions and transcriptional profiles of isolated brain and muscle porcine cells.Scientific reports · 2022Article
- Ursolic acid improves the indoxyl sulfate-induced impairment of mitochondrial biogenesis in C2C12 cells.Nutrition research and practice · 2022Article
- miRNAs as markers for the development of individualized training regimens: A pilot study.Physiological reports · 2022Article
- Therapeutic vs. Suprapharmacological Metformin Concentrations: Different Effects on Energy Metabolism and Mitochondrial Function in Skeletal Muscle CellsFrontiers in pharmacology · 2022Article
- MitomiRs: their roles in mitochondria and importance in cancer cell metabolism.Radiology and oncology · 2021Review
- The mechanism by which noncoding RNAs regulate muscle wasting in cancer cachexia.Precision clinical medicine · 2021Article
- Dysregulation of exosomal miR-192 and miR-194 expression in lung adenocarcinoma patients.Saudi journal of biological sciences · 2021Article
- Integrated Genome-Wide Analysis of MicroRNA Expression Quantitative Trait Loci in Pig Longissimus Dorsi Muscle.Frontiers in genetics · 2021Article
- miR-345-3p serves a protective role during gestational diabetes mellitus by targeting BAK1.Experimental and therapeutic medicine · 2021Article
- Functional Role of circRNAs in the Regulation of Fetal Development, Muscle Development, and Lactation in Livestock.BioMed research international · 2021Review
- Functional mechanism and clinical implications of MicroRNA-423 in human cancers.Cancer medicine · 2020Review
- KAP1-associated transcriptional inhibitory complex regulates C2C12 myoblasts differentiation and mitochondrial biogenesis via miR-133a repression.Cell death & disease · 2020Article
- Identification of the Key Molecular Drivers of Phosphorus Utilization Based on Host miRNA-mRNA and Gut Microbiome Interactions.International journal of molecular sciences · 2020Article
- The long noncoding RNA MyHC IIA/X-AS contributes to skeletal muscle myogenesis and maintains the fast fiber phenotype.The Journal of biological chemistry · 2020Article
- Cellular microRNA-155 Regulates Virus-Induced Inflammatory Response and Protects against Lethal West Nile Virus Infection.Viruses · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our previous study, we identified an miRNA regulatory network involved in energy metabolism in porcine muscle. To better understand the involvement of miRNAs in cellular ATP production and energy metabolism, here we used C2C12 myoblasts, in which ATP levels increase during differentiation, to identify miRNAs modulating these processes. ATP level, miRNA and mRNA microarray expression profiles during C2C12 differentiation into myotubes were assessed. The results suggest 14 miRNAs (miR-423-3p, miR-17, miR-130b, miR-301a/b, miR-345, miR-15a, miR-16a, miR-128, miR-615, miR-1968, miR-1a/b, and miR-194) as cellular ATP regulators targeting genes involved in mitochondrial energy metabolism (Cox4i2, Cox6a2, Ndufb7, Ndufs4, Ndufs5, and Ndufv1) during C2C12 differentiation. Among these, miR-423-3p showed a high inverse correlation with increasing ATP levels. Besides having implications in promoting cell growth and cell cycle progression, its function in cellular ATP regulation is yet unknown. Therefore, miR-423-3p was selected and validated for the function together with its potential target, Cox6a2. Overexpression of miR-423-3p in C2C12 myogenic differentiation lead to decreased cellular ATP level and decreased expression of Cox6a2 compared to the negative control. These results suggest miR-423-3p as a novel regulator of ATP/energy metabolism by targeting Cox6a2.
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