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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 4693703, 16 pages
Research Article

The C-ETS2-TFEB Axis Promotes Neuron Survival under Oxidative Stress by Regulating Lysosome Activity

1Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai 200031, China
2Tianjin Haihe Hospital, Tianjin Institute of Respiratory Diseases, Tianjin 300350, China
3The University of Oklahoma Health Sciences Center, 940 Stanton L. Young Boulevard, BMSB 634a, Oklahoma City, OK 73104, USA
4School of Biological Sciences, The University of Hong Kong, 5N09, Kadoorie Biological Sciences Building, Pokfulam Road, Hong Kong

Received 25 November 2015; Revised 5 February 2016; Accepted 17 February 2016

Academic Editor: Paloma B. Liton

Copyright © 2016 Shumin Ma et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Excessive reactive oxygen species/reactive nitrogen species (ROS/RNS) produced as a result of ageing causes damage to macromolecules and organelles or leads to interference of cell signalling pathways, which in turn results in oxidative stress. Oxidative stress occurs in many neurodegenerative diseases (e.g., Parkinson’s disease) and contributes to progressive neuronal loss. In this study, we show that cell apoptosis is induced by oxidative stress and that lysosomes play an important role in cell survival under oxidative stress. As a compensatory response to this stress, lysosomal genes were upregulated via induction of transcription factor EB (TFEB). In addition, localization of TFEB to the nucleus was increased by oxidative stress. We also confirmed that TFEB protects cells from oxidative stress both in vitro and in vivo. Finally, we found that C-ETS2 senses oxidative stress, activates TFEB transcription, and mediates the upregulation of lysosomal genes. Our results demonstrate a mechanistic pathway for inducing lysosomal activity during ageing and neurodegeneration.