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Article

Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells

  • Authors:
    • Jianhua Wu
    • Fang Wang
    • Zhiqiang Su
    • Jue Liu
    • Sang Hu
    • Hao Li
    • Pei Hu
    • Dongfang Wu
  • View Affiliations / Copyright

    Affiliations: Department of Pharmacy, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China, Department of Pharmacy, The First Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China, Department of Pharmacy, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China
  • Pages: 4280-4285
    |
    Published online on: April 25, 2017
       https://doi.org/10.3892/mmr.2017.6510
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Abstract

Ischemic preconditioning is an endogenous protective mechanism that may be triggered by exposure to hydrogen peroxide (H2O2). However, the exact mechanisms underlying preconditioning remain to be fully understood. Ataxia-telangiectasia mutated (ATM) is regarded as an essential endogenous protective protein against stress. The aim of the present study was therefore to investigate whether ATM mediates H2O2 preconditioning. Preconditioning of Neuro‑2a (N2a) cells with 100 µM H2O2 for 90 min resulted in protection from injury induced by a long period of exposure to 600 µM H2O2. In addition, preconditioning with 100 µM H2O2 activated ATM and increased ATM mRNA and protein expression levels in N2a cells. Furthermore, the protective effects induced by H2O2 preconditioning were attenuated by pretreatment with the ATM inhibitor, Ku55933, or ATM small interfering RNA. In conclusion, these findings suggested that ATM is involved in H2O2 preconditioning‑mediated protection against oxidative stress‑induced injury in N2a cells. To the best of our knowledge, the present study demonstrated, for the first time, that the ATM protein is a key mediator of H2O2 preconditioning.
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Copy and paste a formatted citation
Spandidos Publications style
Wu J, Wang F, Su Z, Liu J, Hu S, Li H, Hu P and Wu D: Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells. Mol Med Rep 15: 4280-4285, 2017.
APA
Wu, J., Wang, F., Su, Z., Liu, J., Hu, S., Li, H. ... Wu, D. (2017). Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells. Molecular Medicine Reports, 15, 4280-4285. https://doi.org/10.3892/mmr.2017.6510
MLA
Wu, J., Wang, F., Su, Z., Liu, J., Hu, S., Li, H., Hu, P., Wu, D."Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells". Molecular Medicine Reports 15.6 (2017): 4280-4285.
Chicago
Wu, J., Wang, F., Su, Z., Liu, J., Hu, S., Li, H., Hu, P., Wu, D."Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells". Molecular Medicine Reports 15, no. 6 (2017): 4280-4285. https://doi.org/10.3892/mmr.2017.6510
Copy and paste a formatted citation
x
Spandidos Publications style
Wu J, Wang F, Su Z, Liu J, Hu S, Li H, Hu P and Wu D: Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells. Mol Med Rep 15: 4280-4285, 2017.
APA
Wu, J., Wang, F., Su, Z., Liu, J., Hu, S., Li, H. ... Wu, D. (2017). Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells. Molecular Medicine Reports, 15, 4280-4285. https://doi.org/10.3892/mmr.2017.6510
MLA
Wu, J., Wang, F., Su, Z., Liu, J., Hu, S., Li, H., Hu, P., Wu, D."Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells". Molecular Medicine Reports 15.6 (2017): 4280-4285.
Chicago
Wu, J., Wang, F., Su, Z., Liu, J., Hu, S., Li, H., Hu, P., Wu, D."Role of ataxia-telangiectasia mutated in hydrogen peroxide preconditioning against oxidative stress in Neuro-2a cells". Molecular Medicine Reports 15, no. 6 (2017): 4280-4285. https://doi.org/10.3892/mmr.2017.6510
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