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Noise exposures causing hearing loss generate proteotoxic stress and activate the proteostasis network

ABSTRACT: Noise exposures causing hearing loss generate proteotoxic stress and activate the proteostasis network

PROVIDER: PRJNA673829 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12964735_1.fastq.gz	Fastqsanger.gz
	SRR12964735_2.fastq.gz	Fastqsanger.gz
	SRR12964736_1.fastq.gz	Fastqsanger.gz
	SRR12964736_2.fastq.gz	Fastqsanger.gz
	SRR12964737_1.fastq.gz	Fastqsanger.gz

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Noise exposures causing hearing loss generate proteotoxic stress and activate the proteostasis network

Project description:We investigate how noise insults affect the cochlea with proteomics and functional assays. Quantitative proteomics reveals that exposure to loud noise causes proteotoxicity. We identify and confirm hundreds of proteins that accumulate, including cytoskeletal proteins, and several nodes of the proteostasis network. Transcriptomic analysis reveals that a subset of the genes encoding these proteins also increase acutely after noise exposure, including numerous proteasome subunits.

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Noise Exposures Causing Hearing Loss Generate Proteotoxic Stress and Activate the Proteostasis Network.

Project description:Exposure to excessive sound causes noise-induced hearing loss through complex mechanisms and represents a common and unmet neurological condition. We investigate how noise insults affect the cochlea with proteomics and functional assays. Quantitative proteomics reveals that exposure to loud noise causes proteotoxicity. We identify and confirm hundreds of proteins that accumulate, including cytoskeletal proteins, and several nodes of the proteostasis network. Transcriptomic analysis reveals that a subset of the genes encoding these proteins also increases acutely after noise exposure, including numerous proteasome subunits. Global cochlear protein ubiquitylation levels build up after exposure to excess noise, and we map numerous posttranslationally modified lysines residues. Several collagen proteins decrease in abundance, and Col9a1 specifically localizes to pillar cell heads. After two weeks of recovery, the cochlea selectively elevates the abundance of the protein synthesis machinery. We report that overstimulation of the auditory system drives a robust cochlear proteotoxic stress response.

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Cochlear single-cell gene expression profiles in mice with noise-induced hidden hearing loss and noise-induced hearing loss.

Project description:Noise-induced hidden hearing loss (HHL) is a new type of hearing loss that has been identified in recent years and leads to insidious damage to the cochlea, unlike the well-known noise-induced hearing loss (NIHL). However, the cellular and molecular basis for it remains to be elucidated. Here, we established a single-cell transcriptome profile of the C57BL/6J mouse cochlea, in which we describe the transcriptome changes of individual cell types within the cochlea with HHL and NIHL. Mice in the HHL group were exposed to 110 dB of noise for 2 hours, and those in the NIHL group were exposed to 115 dB of noise for 4 hours for 3 days. The cochlea was taken 6 hours after the last noise exposure. The control group was not exposed to noise, with other conditions being the same as those in the noise-exposed group. The results of sequencing at the single-cell level help us gain a deeper understanding of the mechanisms of the development of HHL and NIHL.

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Cochlear single-cell gene expression profiles in mice with noise-induced hidden hearing loss and noise-induced hearing loss.

Project description:Cochlear single-cell gene expression profiles in mice with noise-induced hidden hearing loss and noise-induced hearing loss.

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Noise exposures causing hearing loss generate proteotoxic stress and activate the proteostasis network

Project description:Nopporn Jongkamonwiwat, Miguel Ramirez, Ann C.Y. Wong, Yi-Zhi Wang, Jintao Yu, Tirzah Abbott, Allen F. Ryan, Jeffrey N. Savas

2019-12-29 | MSV000084739 | MassIVE

microRNA expression data of ascencding central auditory pathway from noise-induced hearing loss rat model

Project description:115 dB SPL of noise exposure for 2 hours causes high threshold shift at day 1 and recovers rapidly at day 3. Microarray was performed to identify up or down-regulated genes during rapid recovery of hearing.

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Cochlear transcriptome at 3 hours post-noise trauma in mice

Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss in the cochlea (inner ear), transcriptome of the cochlear sample was analyzed after induction of hearing loss by exposure to intense noise in mice. Cochlear transcriptome was analyzed at 3 hours following the noise exposure.

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Cochlear transcriptome after noise trauma and dexamethasone therapy in mice

Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss and dexamethasone therapy in the cochlea (inner ear), transcriptome of cochlear samples was analyzed after induction of hearing loss by exposure to intense noise in mice. Dexamethasone was intraperitoneally injected immediately following the noise trauma. Cochlear transcriptome was analyzed at 12h and 24h following the noise trauma and dexamethasone administration.

2016-12-03 | GSE85290 | GEO

Epigenetic regulation of global proteostasis dynamics by RBBP5 ensures mammalian organismal health

Project description:Proteostasis is vital for cellular health, with disruptions leading to pathologies including aging, neurodegeneration and metabolic disorders. Traditionally, proteotoxic stress responses were studied as acute reactions to various noxious factors; however, recent evidence reveals that many stress-response genes exhibit ~12-hour ultradian rhythms under physiological conditions in mammals. These rhythms, driven by an XBP1s-dependent 12h oscillator, are crucial for managing proteostasis. By exploring the chromatin landscape of the murine 12h hepatic oscillator, we identified RBBP5, a key subunit of the COMPASS complex, as an essential epigenetic regulator of proteostasis. RBBP5 is indispensable for regulating both the hepatic 12h oscillator and transcriptional response to acute proteotoxic stress, acting as a co-activator for master proteostasis transcription factor XBP1s. RBBP5 ablation leads to increased sensitivity to proteotoxic stress, chronic inflammation, and hepatic steatosis in mice, along with impaired autophagy and reduced cell survival in vitro. In humans, lower RBBP5 expression is associated with dampened adaptive stress-response gene expression and hepatic steatosis. Our findings establish RBBP5 as a critical regulator of proteostasis, essential for maintaining mammalian organismal health.

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Apoptotic vesicles resist oxidative damage in noise-induced hearing loss through activation of FOXO3a-SOD2 pathway

Project description:The purpose of this study is to investigate the therapeutic effect of MSC-derived apoVs treatment on NIHL and the potential mechanism of resisting oxidative stress damage in hair cells, as well as the distribution of apoptotic vesicles in the inner ear. The study provided a new direction for the treatment of noise-induced hearing loss and inner ear delivery.

2023-03-20 | PXD040989 |

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