Mitochondrial Peroxiredoxin 3 Regulates Sensory Cell Survival in the Cochlea

被引:38
|
作者
Chen, Fu-Quan [1 ]
Zheng, Hong-Wei [1 ]
Schacht, Jochen [2 ]
Sha, Su-Hua [1 ]
机构
[1] Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA
[2] Univ Michigan, Kresge Hearing Res Inst, Dept Otolaryngol, Ann Arbor, MI 48109 USA
来源
PLOS ONE | 2013年 / 8卷 / 04期
关键词
OXIDATIVE STRESS; HEARING-LOSS; AMINOGLYCOSIDE OTOTOXICITY; IRON CHELATORS; DEATH; MICE; REDUCTION; FAMILY; DAMAGE;
D O I
10.1371/journal.pone.0061999
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
This study delineates the role of peroxiredoxin 3 (Prx3) in hair cell death induced by several etiologies of acquired hearing loss (noise trauma, aminoglycoside treatment, age). In vivo, Prx3 transiently increased in mouse cochlear hair cells after traumatic noise exposure, kanamycin treatment, or with progressing age before any cell loss occurred; when Prx3 declined, hair cell loss began. Maintenance of high Prx3 levels via treatment with the radical scavenger 2,3-dihydroxybenzoate prevented kanamycin-induced hair cell death. Conversely, reducing Prx3 levels with Prx3 siRNA increased the severity of noise-induced trauma. In mouse organ of Corti explants, reactive oxygen species and levels of Prx3 mRNA and protein increased concomitantly at early times of drug challenge. When Prx3 levels declined after prolonged treatment, hair cells began to die. The radical scavenger p-phenylenediamine maintained Prx3 levels and attenuated gentamicin-induced hair cell death. Our results suggest that Prx3 is up-regulated in response to oxidative stress and that maintenance of Prx3 levels in hair cells is a critical factor in their susceptibility to acquired hearing loss.
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页数:10
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