• Celia Zhang, Wei Sun, Ji Li, Binbin Xiong, Mitchell D Frye, Dalian Ding, Richard Salvi, Mi-Jung Kim, Shinichi Someya, and Bo Hua Hu.
• Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: celiazha@buffalo.edu.
• Neuroscience. 2017 Oct 11; 361: 179-191.

AbstractSestrin 2 (SESN2) is a stress-inducible protein that protects tissues from oxidative stress and delays the aging process. However, its role in maintaining the functional and structural integrity of the cochlea is largely unknown. Here, we report the expression of SESN2 protein in the sensory epithelium, particularly in hair cells. Using C57BL/6J mice, a mouse model of age-related cochlear degeneration, we observed a significant age-related reduction in SESN2 expression in cochlear tissues that was associated with early onset hearing loss and accelerated age-related sensory cell degeneration that progressed from the base toward the apex of the cochlea. Hair cell death occurred by caspase-8 mediated apoptosis. Compared to C57BL/6J control mice, Sesn2 KO mice displayed enhanced expression of proinflammatory genes and activation of basilar membrane macrophages, suggesting that loss of SESN2 function provokes the immune response. Together, these results suggest that Sesn2 plays an important role in cochlear homeostasis and immune responses to stress.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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