Abstract
Noise-induced hearing loss (NIHL) is a global occupational disease affecting health. To date, genetic polymorphism studies on NIHL have been performed extensively. However, the proteomic profiles in the cochleae of mice suffering noise damage remain unclear. The goal of this current study was to perform a comprehensive investigation on characterizing protein expression changes in the cochlea based on a mouse model of NIHL using tandem mass tag (TMT)-labeling quantitative proteomics, and to reveal the potential biomarkers and pathogenesis of NIHL. Male C57BL/6J mice were exposed to noise at 120 dB SPL for 4 h to construct the NIHL mouse model. The levels of MDA and SOD, and the production of proinflammatory cytokines including TNF-α and IL-6 in the mice cochleae, were determined using chemical colorimetrical and ELISA kits. Moreover, differentially expressed proteins (DEPs) were validated using Western blotting. The mouse model showed that the ABR thresholds at frequencies of 4, 8, 12, 16, 24 and 32 kHz were significantly increased, and outer hair cells (HCs) showed a distinct loss in the noise-exposed mice. Proteomics analysis revealed that 221 DEPs were associated with NIHL. Bioinformatics analysis showed that a set of key inflammation and autophagy-related DEPs (ITGA1, KNG1, CFI, FGF1, AKT2 and ATG5) were enriched in PI3K/AKT, ECM-receptor interaction, and focal adhesion pathways. The results revealed that the MDA level was significantly increased, but the activity of SOD decreased in noise-exposed mice compared to the control mice. Moreover, TNF-α and IL-6 were significantly increased in the noise-exposed mice. Western blotting revealed that the expression levels of ITGA1, KNG1, and CFI were upregulated, but FGF1, AKT2, and ATG5 were significantly downregulated in noise-exposed mice. This study provides new scientific clues about the future biomarkers and pathogenesis studies underlying NIHL. Furthermore, the findings suggest that the validated DEPs may be valuable biomarkers of NIHL, and inflammation and autophagy may be pivotal mechanisms that underlie NIHL.
Highlights
Noise is a widespread occupational hazard affecting the health of workers
The results revealed that 120 dB sound pressure level (SPL) 4 h noise exposure condition could cause severe Noiseinduced hearing loss (NIHL) and impair the outer hair cells (OHCs)
The results showed that the trend of differentially expressed proteins (DEPs) exhibited a good consistency between the three samples in each group
Summary
Noise is a widespread occupational hazard affecting the health of workers. Noiseinduced hearing loss (NIHL) is a progressive sensorineural hearing loss caused by prolonged noise exposure. NIHL is a major occupational-related disorder and is a hard occupational health issue to solve in workplace safety [1]. It is worth noting that approximately 10% of the world’s population is permanently exposed to high-intensity noise and are at risk of suffering NIHL [2]. NIHL has been the third largest occupational health problem in China, the incidence of which has been increasing [3]. NIHL is an extremely complex neurological hearing impairment caused by a variety of environmental and genetic factors. Oxidative stress is thought to be involved in the occurrence and development of NIHL by inducing hair cells (HCs) loss in the inner ear [4]
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