FBXO3 Downregulation Attenuates Noise-induced Hearing Loss by Suppressing ATG10 Degradation and Activating Autophagy

2020 ◽  
Author(s):  
Fan Ye ◽  
Bi Lin ◽  
Lian Fang
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Underlying Mechanism ◽  
Noise Induced Hearing Loss ◽  
Age Related ◽  
Rat Cochlea ◽  
Model Treatment ◽  
Ear Injury ◽  
Age Related Hearing Loss

Abstract Noise induced hearing loss (NIHL) is a kind of hearing impairment, which is next to the age-related hearing loss. More and more evidences have verified that overproduction of reactive oxygen species is a common pathologic phenomenon of different inner ear injury including NIHL, and autophagy contributes to attenuate NIHL by reducing oxidative stress. However, the underlying mechanism by which noise exposure causes autophagy activation remains unclear. In this study, we found that NIHL was accompanied by autophagy in the rat cochlea. Furthermore, twelve common genes were found at the GEO datasets GSE85290 and GSE8342, and E3 ubiquitination ligase FBXO3 was confirmed significantly reduced in NIHL rat cochlea. Next, we demonstrated that FBXO3 can directly binding with autophagy-related protein 10 (ATG10), which is necessary for the initiation of autophagy, and mediate its degradation. In vivo animal model treatment with rapamycin, an autophagy activator, significantly reduced the NIHL. Based on these data, we confirmed that FBXO3 played an important role in autophagy caused by NIHL, may be a potential target of NIHL treatment.

scholarly journals Occupational Exposure to Noise and Age-related Hearing Loss in an Elderly Population of Southern Italy

2020 ◽  
Vol 13 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Luigi De Maria ◽  
Antonio Caputi ◽  
Rodolfo Sardone ◽  
Enza Sabrina Silvana Cannone ◽  
Francesca Mansi ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Occupational Exposure ◽  
Elderly Population ◽  
Noise Exposure ◽  
Exposed Population ◽  
Age Related ◽  
Age Dependent ◽  
Occupationally Exposed ◽  
Age Related Hearing Loss

Background: Age-Related Hearing Loss (ARHL) is a gradual and irreversible age-dependent decline in auditory function. There is still no consensus on the long-term functional effects of noise exposure on ARHL. Objective: This study aimed to compare the prevalence of ARHL in an elderly population occupationally exposed to noise in a non-exposed population. Methods: The population was divided into two groups: a group of 482 subjects professionally exposed to noise for over 10 years and a group of 1129 non-exposed subjects. Among the exposed subjects, a subgroup of 298 who worked for over 10 years in the glassware industry was selected. All the participants underwent a thorough otorhinolaryngological examination. Results: The presence of ARHL was found in 81% of exposed subjects and in 4% of non-exposed subjects. In the sub-group of glassware workers, the prevalence was 88%. The statistical analysis showed a significant association between previous occupational exposure to noise and ARHL (OR = 1.09; 95% CI = 1.067-1.124; p = 0.0012) and between exposure to the glassware industry and ARHL (OR = 1.89; 95% CI = 1.78-1.96; p = 0.006). Conclusion: Consistent with recent studies, we found a significantly higher prevalence of ARHL among workers exposed to noise; however, further studies are needed to support these findings.

scholarly journals Noise-Induced Cochlear Damage Involves PPAR Down-Regulation through the Interplay between Oxidative Stress and Inflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1188
Author(s):  
Fabiola Paciello ◽  
Anna Pisani ◽  
Rolando Rolesi ◽  
Vincent Escarrat ◽  
Jacopo Galli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Noise Exposure ◽  
Negative Control ◽  
In Vivo Model ◽  
Noise Induced Hearing Loss ◽  
Down Regulation ◽  
Anti Inflammatory ◽  
Cochlear Dysfunction

The cross-talk between oxidative stress and inflammation seems to play a key role in noise-induced hearing loss. Several studies have addressed the role of PPAR receptors in mediating antioxidant and anti-inflammatory effects and, although its protective activity has been demonstrated in several tissues, less is known about how PPARs could be involved in cochlear dysfunction induced by noise exposure. In this study, we used an in vivo model of noise-induced hearing loss to investigate how oxidative stress and inflammation participate in cochlear dysfunction through PPAR signaling pathways. Specifically, we found a progressive decrease in PPAR expression in the cochlea after acoustic trauma, paralleled by an increase in oxidative stress and inflammation. By comparing an antioxidant (Q-ter) and an anti-inflammatory (Anakinra) treatment, we demonstrated that oxidative stress is the primary element of damage in noise-induced cochlear injury and that increased inflammation can be considered a consequence of PPAR down-regulation induced by ROS production. Indeed, by decreasing oxidative stress, PPARs returned to control values, reactivating the negative control on inflammation in a feedback loop.

Impulse noise exposure in early adulthood accelerates age-related hearing loss

2013 ◽  
Vol 271 (6) ◽  
pp. 1351-1354 ◽  
Author(s):  
Min Xiong ◽  
Chuanhong Yang ◽  
Huangwen Lai ◽  
Jian Wang
Keyword(s):  
Hearing Loss ◽  
Impulse Noise ◽  
Noise Exposure ◽  
Early Adulthood ◽  
Age Related ◽  
Age Related Hearing Loss

scholarly journals Workplace noise exposure and the prevalence and 10-year incidence of age-related hearing loss

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0255356
Author(s):  
Bamini Gopinath ◽  
Catherine McMahon ◽  
Diana Tang ◽  
George Burlutsky ◽  
Paul Mitchell
Keyword(s):  
Older Adults ◽  
Hearing Loss ◽  
Noise Exposure ◽  
Later Life ◽  
Occupational Noise ◽  
Severe Hearing Loss ◽  
Occupational Noise Exposure ◽  
Age Related ◽  
Age Related Hearing Loss ◽  
Workplace Noise

There is paucity of population-based data on occupational noise exposure and risk of age-related hearing loss. Therefore, we assessed cross-sectional and longitudinal associations of past workplace noise exposure with hearing loss in older adults. At baseline, 1923 participants aged 50+ years with audiological and occupational noise exposure data included for analysis. The pure-tone average of frequencies 0.5, 1.0, 2.0 and 4.0 kHz (PTA0.5-4KHz) >25 dB HL in the better ear, established the presence of hearing loss. Participants reported exposure to workplace noise, and the severity and duration of this exposure. Prior occupational noise exposure was associated with a 2-fold increased odds of moderate-to-severe hearing loss: multivariable-adjusted OR 2.35 (95% CI 1.45–3.79). Exposure to workplace noise for >10 years increased the odds of having any hearing loss (OR 2.39, 95% CI 1.37–4.19) and moderate-to-severe hearing loss (OR 6.80, 95% CI 2.97–15.60). Among participants reporting past workplace noise exposure at baseline the 10-year incidence of hearing loss was 35.5% versus 29.1% in those who had no workplace noise exposure. Workplace noise exposure was associated with a greater risk of incident hearing loss during the 10-year follow-up: multivariable-adjusted OR 1.39 (95% CI 1.13–1.71). Prior occupational noise exposure was not associated with hearing loss progression. Workplace noise exposure increased the risk of incident hearing loss in older adults. Our findings underscore the importance of preventive measures which diminish noise exposure in the workplace, which could potentially contribute towards reducing the burden of hearing loss in later life.

scholarly journals Exacerbated age-related hearing loss in mice lacking the p43 mitochondrial T3 receptor

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Corentin Affortit ◽  
François Casas ◽  
Sabine Ladrech ◽  
Jean-Charles Ceccato ◽  
Jérôme Bourien ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Spiral Ganglion ◽  
Electrophysiological Recording ◽  
Mitochondrial Activity ◽  
P53 Expression ◽  
Age Related ◽  
Hearing Function ◽  
Ganglion Neurons ◽  
Age Related Hearing Loss

Abstract Background Age-related hearing loss (ARHL), also known as presbycusis, is the most common sensory impairment seen in elderly people. However, the cochlear aging process does not affect people uniformly, suggesting that both genetic and environmental (e.g., noise, ototoxic drugs) factors and their interaction may influence the onset and severity of ARHL. Considering the potential links between thyroid hormone, mitochondrial activity, and hearing, here, we probed the role of p43, a N-terminally truncated and ligand-binding form of the nuclear receptor TRα1, in hearing function and in the maintenance of hearing during aging in p43−/− mice through complementary approaches, including in vivo electrophysiological recording, ultrastructural assessments, biochemistry, and molecular biology. Results We found that the p43−/− mice exhibit no obvious hearing loss in juvenile stages, but that these mice developed a premature, and more severe, ARHL resulting from the loss of cochlear sensory outer and inner hair cells and degeneration of spiral ganglion neurons. Exacerbated ARHL in p43−/− mice was associated with the early occurrence of a drastic fall of SIRT1 expression, together with an imbalance between pro-apoptotic Bax, p53 expression, and anti-apoptotic Bcl2 expression, as well as an increase in mitochondrial dysfunction, oxidative stress, and inflammatory process. Finally, p43−/− mice were also more vulnerable to noise-induced hearing loss. Conclusions These results demonstrate for the first time a requirement for p43 in the maintenance of hearing during aging and highlight the need to probe the potential link between human THRA gene polymorphisms and/or mutations and accelerated age-related deafness or some adult-onset syndromic deafness.

Medical-Legal Assessment of Hearing Loss

1995 ◽  
Vol 112 (5) ◽  
pp. P75-P75
Author(s):  
Robert A. Dobie
Keyword(s):  
Hearing Loss ◽  
Time Course ◽  
Noise Induced Hearing Loss ◽  
Educational Objectives ◽  
Legal Assessment ◽  
Epidemiologic Data ◽  
Age Related ◽  
Exposure History ◽  
Age Related Hearing Loss

Educational objectives: To understand the epidemiology of noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL), including time course, interactions, and importance of occupational and nonoccupational exposure history; to use clinical and epidemiologic data and principles to diagnose NIHL and ARHL; and to estimate the relative contributions of each in individual cases.

Genetics of age-related hearing loss in mice. III. Susceptibility of inbred and F1 hybrid strains to noise-induced hearing loss

1996 ◽  
Vol 93 (1-2) ◽  
pp. 181-187 ◽  
Author(s):  
Lawrence C. Erway ◽  
Yea-Wen Shiau ◽  
Rickie R. Davis ◽  
Edward F. Krieg
Keyword(s):  
Hearing Loss ◽  
Noise Induced Hearing Loss ◽  
F1 Hybrid ◽  
Age Related ◽  
Age Related Hearing Loss

Age-Related and Noise-Induced Hearing Loss

2018 ◽  
pp. 162-188
Author(s):  
Ruili Xie ◽  
Tessa-Jonne F. Ropp ◽  
Michael R. Kasten ◽  
Paul B. Manis
Keyword(s):  
Hearing Loss ◽  
Auditory Nerve ◽  
Transmitter Release ◽  
Time Course ◽  
Functional Change ◽  
Noise Induced Hearing Loss ◽  
Nerve Activity ◽  
Auditory Periphery ◽  
Age Related ◽  
Age Related Hearing Loss

Hearing loss generally occurs in the auditory periphery but leads to changes in the central auditory system. Noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) affect neurons in the ventral cochlear nucleus (VCN) at both the cellular and systems levels. In response to a decrease in auditory nerve activity associated with hearing loss, the large synaptic endings of the auditory nerve, the endbulbs of Held, undergo simplification of their structure and the volume of the postsynaptic bushy neurons decreases. A major functional change shared by NIHL and ARHL is the development of asynchronous transmitter release at endbulb synapses during periods of high afferent firing. Compensatory adjustements in transmitter release, including changes in release probability and quantal content, have also been reported. The excitability of the bushy cells undergoes subtle changes in the long-term, although short-term, reversible changes in excitability may also occur. These changes are not consistently observed across all models of hearing loss, suggesting that the time course of hearing loss, and potential developmental effects, may influence endbulb transmission in multiple ways. NIHL can alter the representation of the loudness of tonal stimuli by VCN neurons and is accompanied by changes in spontaneous activity in VCN neurons. However, little is known about the representation of more complex stimuli. The relationship between mechanistic changes in VCN neurons with noise-induced or age-related hearing loss, the accompanying change in sensory coding, and the reversibility of changes with the reintroduction of auditory nerve activity are areas that deserve further thoughtful exploration.

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