The impact of mitochondrial energetic dysfunction on apoptosis in outer hair cells of the cochlea following exposure to intense noise

Hu, Bo; Henderson, Donald; Yang, Wei

doi:10.1016/j.heares.2007.11.002

Cited by 21 publications

(15 citation statements)

References 30 publications

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“…Cisplatin significantly increased the active caspase-3 and Bax protein expression, but decreased Bcl-2 protein expression in the rat cochleae [32], which was in line with our study. Noise exposure results in hair cell death primarily through apoptosis [33]. Several noise-induced events, including calcium influx, ATP depletion, and oxidative stress, play a role in exacerbating the pathological responses of sensory cells [34].…”

Section: Control Cisplatin Model Relative Protein Expressionmentioning

confidence: 99%

Up-regulation of autophagy and apoptosis of cochlear hair cells in mouse models for deafness

Cheng

Yan

2021

Arch Med Sci

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Introduction: Hearing loss is one of the most common sensory disorders. Recent findings have shown that the apoptotic program and autophagy are related to hearing loss. The aim of study was to explore the effects of noise and cisplatin exposure on apoptosis and autophagy in the hair cells of the cochleae. Material and methods: C57BL/6 mice were randomly divided into 3 groups (n = 10 for each): the control group, the noise model group and the cisplatin model group. Auditory brainstem response (ABR) measurements were used to detect the hearing thresholds. TUNEL assay was used to evaluate cell apoptosis. Western blot and immunofluorescence were performed to examine the apoptosis-and autophagy-related proteins. Results: The mice exhibited substantial hearing loss after noise and cisplatin exposure. Additionally, more TUNEL positive cells were observed in the mice after noise and cisplatin exposure compared with the control group. Moreover, the protein expression levels of Beclin-1, LC3-II, Bax and cleaved caspase-3 were significantly increased, while the expression of Bcl-2 was notably decreased in the cochlea after noise (p = 0.0278, 0.0075, 0.0142, 0.0158, 0.0131 respectively) and cisplatin (p = 0.0220, 0.0075, 0.0024, 0.0161, 0.0452 respectively) exposure compared with the control group. Besides, the ratio of LC3-II/LC3-I was substantially higher in the mice treated by cisplatin (p = 0.0046) and noise (p = 0.0220) compared with the control group. Conclusions: Our findings demonstrated for the first time that noise and cisplatin exposure promoted apoptosis and autophagy in the hair cells of the cochleae. This study provides new insights into the mechanisms of noise-or cisplatin-induced hearing loss.

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Section: Control Cisplatin Model Relative Protein Expressionmentioning

confidence: 99%

Up-regulation of autophagy and apoptosis of cochlear hair cells in mouse models for deafness

Cheng

Yan

2021

Arch Med Sci

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“…ROS accumulation and mitochondrial dysfunction have been reported to be involved in HC apoptosis (Hu et al, 2008;He et al, 2016). ROS accumulation leads to mitochondrial depolarization, which results in a decrease in the MMP and the subsequent release of apoptotic factors.…”

Section: Discussionmentioning

confidence: 99%

Blebbistatin Inhibits Neomycin-Induced Apoptosis in Hair Cell-Like HEI-OC-1 Cells and in Cochlear Hair Cells

Gao

Cheng

Wang

et al. 2020

Front. Cell. Neurosci.

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Aging, noise, and ototoxic drug-induced hair cell (HC) loss are the major causes of sensorineural hearing loss. Aminoglycoside antibiotics are commonly used in the clinic, but these often have ototoxic side effects due to the accumulation of oxygen-free radicals and the subsequent induction of HC apoptosis. Blebbistatin is a myosin II inhibitor that regulates microtubule assembly and myosin-actin interactions, and most research has focused on its ability to modulate cardiac or urinary bladder contractility. By regulating the cytoskeletal structure and reducing the accumulation of reactive oxygen species (ROS), blebbistatin can prevent apoptosis in many different types of cells. However, there are no reports on the effect of blebbistatin in HC apoptosis. In this study, we found that the presence of blebbistatin significantly inhibited neomycin-induced apoptosis in HC-like HEI-OC-1 cells. We also found that blebbistatin treatment significantly increased the mitochondrial membrane potential (MMP), decreased ROS accumulation, and inhibited pro-apoptotic gene expression in both HC-like HEI-OC-1 cells and explant-cultured cochlear HCs after neomycin exposure. Meanwhile, blebbistatin can protect the synaptic connections between HCs and cochlear spiral ganglion neurons. This study showed that blebbistatin could maintain mitochondrial function and reduce the ROS level and thus could maintain the viability of HCs after neomycin exposure and the neural function in the inner ear, suggesting that blebbistatin has potential clinic application in protecting against ototoxic drug-induced HC loss.

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“…Mitochondria are specialized organelles that produce most of the cell's energy (Alberts et al , ). Changes in mitochondrial respiration (Hu et al , ; Crawley & Keithley, ; Park et al , ) and activation of a mitochondrial cell death pathway (Wang et al , ) have been reported in mammalian hair cells following sound trauma. Additionally, the transcript encoding C14orf159 is up‐regulated in S .…”

Section: Discussionmentioning

confidence: 99%

“…Mitochondria are specialized organelles that produce most of the cell's energy (Alberts et al, 2008). Changes in mitochondrial respiration (Hu et al, 2008;Crawley & Keithley, 2011;Park et al, 2012) and activation of a mitochondrial cell death pathway (Wang et al, 2007) have been reported in mammalian hair cells following sound trauma. Additionally, the transcript encoding C14orf159 is up-regulated in S. salar gill affected by amoebic gill disease immediately following exposure to virulent amoebae (Morrison et al, 2006), and the human c14orf159 gene is known to bind ER in 17 -oestradiol-treated human breast cancer cells (Creekmore et al, 2007).…”

Section: S T Ru C T U R a L G E N E Smentioning

confidence: 99%

Identification of a gene set to evaluate the potential effects of loud sounds from seismic surveys on the ears of fishes: a study with Salmo salar

Andrews

Payne

Rise

2014

Journal of Fish Biology

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Functional genomic studies were carried out on the inner ear of Atlantic salmon Salmo salar following exposure to a seismic airgun. Microarray analyses revealed 79 unique transcripts (passing background threshold), with 42 reproducibly up-regulated and 37 reproducibly down-regulated in exposed v. control fish. Regarding the potential effects on cellular energetics and cellular respiration, altered transcripts included those with roles in oxygen transport, the glycolytic pathway, the Krebs cycle and the electron transport chain. Of these, a number of transcripts encoding haemoglobins that are important in oxygen transport were up-regulated and among the most highly expressed. Up-regulation of transcripts encoding nicotinamide riboside kinase 2, which is also important in energy production and linked to nerve cell damage, points to evidence of neuronal damage in the ear following noise exposure. Transcripts related to protein modification or degradation also indicated potential damaging effects of sound on ear tissues. Notable in this regard were transcripts associated with the proteasome–ubiquitin pathway, which is involved in protein degradation, with the transcript encoding ubiquitin family domain-containing protein 1 displaying the highest response to exposure. The differential expression of transcripts observed for some immune responses could potentially be linked to the rupture of cell membranes. Meanwhile, the altered expression of transcripts for cytoskeletal proteins that contribute to the structural integrity of the inner ear could point to repair or regeneration of ear tissues including auditory hair cells. Regarding potential effects on hormones and vitamins, the protein carrier for thyroxine and retinol (vitamin A), namely transthyretin, was altered at the transcript expression level and it has been suggested from studies in mammalian systems that retinoic acid may play a role in the regeneration of damaged hair cells. The microarray experiment identified the transcript encoding growth hormone I as up-regulated by loud sound, supporting previous evidence linking growth hormone to hair cell regeneration in fishes. Quantitative (q) reverse transcription (RT) polymerase chain reaction (qRT-PCR) analyses confirmed dysregulation of some microarray-identified transcripts and in some cases revealed a high level of biological variability in the exposed group. These results support the potential utility of molecular biomarkers to evaluate the effect of seismic surveys on fishes with studies on the ears being placed in a priority category for development of exposure–response relationships. Knowledge of such relationships is necessary for addressing the question of potential size of injury zones.

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The impact of mitochondrial energetic dysfunction on apoptosis in outer hair cells of the cochlea following exposure to intense noise

Cited by 21 publications

References 30 publications

Up-regulation of autophagy and apoptosis of cochlear hair cells in mouse models for deafness

Up-regulation of autophagy and apoptosis of cochlear hair cells in mouse models for deafness

Blebbistatin Inhibits Neomycin-Induced Apoptosis in Hair Cell-Like HEI-OC-1 Cells and in Cochlear Hair Cells

Identification of a gene set to evaluate the potential effects of loud sounds from seismic surveys on the ears of fishes: a study with Salmo salar

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