Open Access

Elucidation of the mechanism of miR‑122‑5p in mediating FOXO3 injury and apoptosis of mouse cochlear hair cells induced by hydrogen peroxide

  • Authors:
    • Jiajun Chen
    • Jixin Qin
    • Jin Liu
  • View Affiliations

  • Published online on: May 9, 2022     https://doi.org/10.3892/etm.2022.11362
  • Article Number: 435
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Unveiling the mechanism of miR‑122‑5p in the mediation of forkhead box O3 (FOXO3) in regards to cochlear hair cell damage provides an effective solution for the treatment of ear hearing disorders. An oxidative stress model using a mouse cochlear hair cell line (HEI‑OC1) was established via hydrogen peroxide (H2O2). Then HEI‑OC1 cells were transfected with miR‑122‑5p mimic, miR‑122‑5p inhibitor, and lentiviral vector FOXO3‑WT/MUT. Cell viability and apoptosis rate were determined by MTT assay and flow cytometry. Reactive oxygen species (ROS) were observed by confocal laser scanning microscopy. Bcl‑2, Bax, capase‑3 and c‑caspase‑9 levels were quantified by western blot analysis and quantitative reverse transcription polymerase chain reaction (RT‑qPCR). Enzyme‑linked immunosorbent assay (ELISA) was used to detect superoxide dismutase (SOD) and malondialdehyde (MDA) levels, and flow cytometry was performed to measure the mitochondrial membrane potential levels. In the HEI‑OC1 oxidative stress model after transfection, the miR‑122‑5p level was decreased, whereas the FOXO3 level was increased, Moreover, the increased FOXO3 level diminished the cell viability, but promoted cell apoptosis. Apart from this, the Bcl‑2 level was downregulated, while levels of Bax, c‑caspase‑3, c‑caspase‑9, ROS and MDA were upregulated. Meanwhile, the mitochondrial membrane potential level was also elevated. Overexpression of miR‑122‑5p was able to partially offset the effects of FOXO3 in the H2O2‑treated HEI‑OC1 cells. Collectively, miR‑122‑5p restrained the decrease in HEI‑OC1 cell viability and apoptosis induced by treatment with H2O2.

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June-2022
Volume 23 Issue 6

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Online ISSN:1792-1015

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Spandidos Publications style
Chen J, Qin J and Liu J: Elucidation of the mechanism of miR‑122‑5p in mediating FOXO3 injury and apoptosis of mouse cochlear hair cells induced by hydrogen peroxide. Exp Ther Med 23: 435, 2022
APA
Chen, J., Qin, J., & Liu, J. (2022). Elucidation of the mechanism of miR‑122‑5p in mediating FOXO3 injury and apoptosis of mouse cochlear hair cells induced by hydrogen peroxide. Experimental and Therapeutic Medicine, 23, 435. https://doi.org/10.3892/etm.2022.11362
MLA
Chen, J., Qin, J., Liu, J."Elucidation of the mechanism of miR‑122‑5p in mediating FOXO3 injury and apoptosis of mouse cochlear hair cells induced by hydrogen peroxide". Experimental and Therapeutic Medicine 23.6 (2022): 435.
Chicago
Chen, J., Qin, J., Liu, J."Elucidation of the mechanism of miR‑122‑5p in mediating FOXO3 injury and apoptosis of mouse cochlear hair cells induced by hydrogen peroxide". Experimental and Therapeutic Medicine 23, no. 6 (2022): 435. https://doi.org/10.3892/etm.2022.11362