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MiR-34a is Involved in the Decrease of ATP Contents Induced by Resistin Through Target on ATP5S in HepG2 Cells

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Abstract

Resistin is associated with metabolic syndrome and deciphering its developmental and molecular mechanisms may help the development of new treatments. MiRNAs serve as negative regulators in many physiological and pathological processes. Here, miRNA microarrays were used to detect differences in expression between resistin-treated and control mice, and results showed miR-34a to be upregulated by resistin. The purpose of this study was to determine whether miR-34a played a role in resistin-induced decrease of ATP contents. Transient transfection of miR-34a mimics was used to overexpress miR-34a and quantitative RT-PCR was used to detect its expression. Western blot analysis was used to determine the rate of expression at the protein level. ATP content was measured using an ATP assay kit. The target gene of miR-34a was analyzed using bioinformatics and confirmed with dual-luciferase report system. MiR-34a was upregulated by resistin in HepG2 cells, and overexpression of miR-34a was found to diminish ATP levels significantly. This study is the first to show that ATP5S is one of the target genes of miR-34a. Resistin diminishes ATP content through the targeting of ATP5S mRNA 3′UTR by miR-34a.

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Acknowledgments

This work was supported by the Program of National Natural Science Foundation of China (31301940, 41301051).

Author Contributions

Fengyun Wen and Bi Li contributed to research data, discussion, and preparation of the manuscript and are the guarantors of this work. As such, they had full access to all study data. They take responsibility for the data’s integrity and accuracy. Zhiguo Wei and Haiwei Zhang contributed to cellular experiments. Chunyan Huang, Yingying Zhou, and Jianyu Liu contributed to the study design.

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No conflicts of interest relevant to this article are exist.

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Wen, F., Li, B., Huang, C. et al. MiR-34a is Involved in the Decrease of ATP Contents Induced by Resistin Through Target on ATP5S in HepG2 Cells. Biochem Genet 53, 301–309 (2015). https://doi.org/10.1007/s10528-015-9693-x

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  • DOI: https://doi.org/10.1007/s10528-015-9693-x

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