Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling

  • Authors:
    • Yan Jiang
    • Wei Wang
    • Zong‑Yang Liu
    • Yi Xie
    • Yuan Qian
    • Xue‑Ni Cai
  • View Affiliations

  • Published online on: November 8, 2017     https://doi.org/10.3892/etm.2017.5465
  • Pages:1021-1028
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Abstract

Tumor necrosis factor (TNF)‑α has been reported to be important in glomerulonephritis, which is closely associated with podocyte dysfunction and apoptosis. However, the precise mechanisms by which TNF‑α expression are regulated remain unclear. The purpose of the present study was to investigate the role of microRNA (miR)‑130a‑3p/301a‑3p in the post‑transcriptional control of TNF‑α expression and high glucose (HG)‑induced podocyte dysfunction. Mice MPC5 podocytes were incubated with HG and transfected with miR‑130a‑3p/301a‑3p mimics or inhibitors, reactive oxygen species (ROS) levels were measured by flow cytometry assay, and the mRNA and protein levels were assayed by using reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and verified using a dual luciferase reporter assay. It was observed that miR‑130a‑3p/301a‑3p was a novel regulator of TNF‑α in mouse podocytes. miR‑130a‑3p/301a‑3p mimics inhibited TNF‑α 3'‑untranslated region luciferase reporter activity, in addition to endogenous TNF‑α protein expression. Furthermore, forced expression of miR‑130a‑3p or miR‑301a‑3p resulted in the downregulation of ROS and malondialdehyde (MDA) and the upregulation of superoxide dismutase (SOD) 1 in the presence of HG. Inhibition of TNF‑α level prevented a remarkable reduc­tion in SOD activity and a marked increase in ROS and MDA levels in HG‑treated podocytes. Furthermore, TNF‑α loss‑of‑function significantly reversed HG‑induced podocyte apoptosis. These data demonstrated a novel up‑stream role for miR‑130a‑3p/301a‑3p in TNF‑α‑mediated podocyte dysfunction and apoptosis in the presence of HG.

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January 2018
Volume 15 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

2016 Impact Factor: 1.261
Ranked #50/128 Medicine Research and Experimental
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APA
Jiang, Y., Wang, W., Liu, Z., Xie, Y., Qian, Y., & Cai, X. (2018). Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling. Experimental and Therapeutic Medicine, 15, 1021-1028. https://doi.org/10.3892/etm.2017.5465
MLA
Jiang, Y., Wang, W., Liu, Z., Xie, Y., Qian, Y., Cai, X."Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling". Experimental and Therapeutic Medicine 15.1 (2018): 1021-1028.
Chicago
Jiang, Y., Wang, W., Liu, Z., Xie, Y., Qian, Y., Cai, X."Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling". Experimental and Therapeutic Medicine 15, no. 1 (2018): 1021-1028. https://doi.org/10.3892/etm.2017.5465