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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 7263736, 13 pages
Research Article

HDAC6 Regulates the Chaperone-Mediated Autophagy to Prevent Oxidative Damage in Injured Neurons after Experimental Spinal Cord Injury

1Department of Rehabilitation, First Affiliated Hospital of Soochow University, Suzhou 215006, China
2Institute of Neuroscience, Soochow University, Suzhou 215123, China
3Department of Orthopaedics, First Affiliated Hospital of Soochow University, Suzhou 215006, China
4Institute for Cardiovascular Science, Soochow University, Suzhou 215006, China

Received 8 March 2015; Revised 10 July 2015; Accepted 22 July 2015

Academic Editor: Adam J. Case

Copyright © 2016 Min Su 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.


Hypoxia-ischemia- (HI-) induced oxidative stress plays a role in secondary pathocellular processes of acute spinal cord injury (SCI) due to HI from many kinds of mechanical trauma. Increasing evidence suggests that the histone deacetylase-6 (HDAC6) plays an important role in cell homeostasis in both physiological and abnormal, stressful, pathological conditions. This paper found that inhibition of HDAC6 accelerated reactive oxygen species (ROS) generation and cell apoptosis in response to the HI. Deficiency of HDAC6 hindered the chaperone-mediated autophagy (CMA) activity to resistance of HI-induced oxidative stress. Furthermore, this study provided the experimental evidence for the potential role of HDAC6 in the regulation of CMA by affecting HSP90 acetylation. Therefore, HDAC6 plays an important role in the function of CMA pathway under the HI stress induced by SCI and it may be a potential therapeutic target in acute SCI model.