Knockdown of peroxiredoxin V increases glutamate‑induced apoptosis in HT22 hippocampal neuron cells

  • Authors:
    • Gui‑Nan Shen
    • Lei Liu
    • Li Feng
    • Yu Jin
    • Mei‑Hua Jin
    • Ying‑Hao Han
    • Cheng‑Hao Jin
    • Yong‑Zhe Jin
    • Dong‑Soek Lee
    • Tae Ho Kwon
    • Yu‑Dong Cui
    • Hu‑Nan Sun
  • View Affiliations

  • Published online on: March 29, 2018     https://doi.org/10.3892/mmr.2018.8826
  • Pages: 7827-7834
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Abstract

High concentrations of glutamate may mediate neuronal cell apoptosis by increasing intracellular reactive oxygen species (ROS) levels. Peroxiredoxin V (Prx V), a member of the Prx family, serves crucial roles in protecting cells from oxidative stress. The present study investigated the regulatory effect of Prx V on glutamate‑induced effects on viability and apoptosis in HT22 cells. Western blotting was used for protein expression analysis and Annexin V/PI staining and flow cytometry for determination of apoptosis. The results demonstrated that glutamate may ROS‑dependently increase HT22 cell apoptosis and upregulate Prx V protein levels. Furthermore, knockdown of Prx V protein expression with a lentivirus significantly enhanced HT22 cell apoptosis mediated by glutamate, which was reversed by inhibition of ROS with N‑acetyl‑L‑cysteine. Inhibiting the extracellular signal‑regulated kinase (ERK) signaling pathway with PD98059, a specific inhibitor for ERK phosphorylation, markedly decreased glutamate‑induced HT22 cell apoptosis in Prx V knockdown cells, indicating the potential involvement of ERK signaling in glutamate‑induced HT22 cell apoptosis. In addition, an increase in nuclear apoptosis‑inducing factor was observed in Prx V knockdown HT22 cells following glutamate treatment, compared with mock cells, whereas no differences in B‑cell lymphoma‑2 and cleaved‑caspase‑3 protein expression levels were observed between mock and Prx V knockdown cells. The results of the present study indicated that Prx V may have potential as a therapeutic molecular target for glutamate‑induced neuronal cell death and provide novel insight into the role of Prx V in oxidative‑stress induced neuronal cell death.
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June-2018
Volume 17 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Shen GN, Liu L, Feng L, Jin Y, Jin MH, Han YH, Jin CH, Jin YZ, Lee DS, Kwon T, Kwon T, et al: Knockdown of peroxiredoxin V increases glutamate‑induced apoptosis in HT22 hippocampal neuron cells. Mol Med Rep 17: 7827-7834, 2018
APA
Shen, G., Liu, L., Feng, L., Jin, Y., Jin, M., Han, Y. ... Sun, H. (2018). Knockdown of peroxiredoxin V increases glutamate‑induced apoptosis in HT22 hippocampal neuron cells. Molecular Medicine Reports, 17, 7827-7834. https://doi.org/10.3892/mmr.2018.8826
MLA
Shen, G., Liu, L., Feng, L., Jin, Y., Jin, M., Han, Y., Jin, C., Jin, Y., Lee, D., Kwon, T., Cui, Y., Sun, H."Knockdown of peroxiredoxin V increases glutamate‑induced apoptosis in HT22 hippocampal neuron cells". Molecular Medicine Reports 17.6 (2018): 7827-7834.
Chicago
Shen, G., Liu, L., Feng, L., Jin, Y., Jin, M., Han, Y., Jin, C., Jin, Y., Lee, D., Kwon, T., Cui, Y., Sun, H."Knockdown of peroxiredoxin V increases glutamate‑induced apoptosis in HT22 hippocampal neuron cells". Molecular Medicine Reports 17, no. 6 (2018): 7827-7834. https://doi.org/10.3892/mmr.2018.8826