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Therapeutic Restoration of miR-96 Prevents Hearing Loss in Mice through Modulation of Noise-Induced and Genetic Pathways

ABSTRACT: Therapeutic Restoration of miR-96 Prevents Hearing Loss in Mice through Modulation of Noise-Induced and Genetic Pathways

PROVIDER: PRJNA1038749 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26784400_1.fastq.gz	Fastqsanger.gz
	SRR26784400_2.fastq.gz	Fastqsanger.gz
	SRR26784401_1.fastq.gz	Fastqsanger.gz
	SRR26784401_2.fastq.gz	Fastqsanger.gz
	SRR26784402_1.fastq.gz	Fastqsanger.gz

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Therapeutic Restoration of miR-96 Prevents Hearing Loss in Mice through Modulation of Noise-Induced and Genetic Pathways

Project description:Hearing loss often arises from impairments in multiple genes, complicating therapeutic development. MicroRNAs, as master regulators, offer promising targets for complex diseases. We explored miR-96’s roles in hair cell (HC) function and noise-induced hearing loss (NIHL), finding that miR-96-/-, not miR-96+/-, mice exhibited progressive hearing loss due to gene regulatory network dysregulation from miR-96 loss in HCs not spiral ganglion neurons (SGNs). Viral-mediated delivery of miR-96 into the inner ear partially rescued hearing of miR-96-/- mice. Tamoxifen-induced depletion of miR-96 in adult UBCCreERT2/+; miR-96fl/fl mice led to hearing loss, with Bach2, Gabra2, Gabra4, Grk1 up-regulation, and Tnn, Col11a1, Gjb3 and Hnf4a down-regulation. Furthermore, noise trauma reduced miR-96, altering Bach2, Bcl2l1, Slc26a9, Gabrb1, Grk1, Nos2 and Cyp1a1 expression, while miR-96 overexpression protected hearing against noise by reversing the expression of Bach2, Bcl2l1 and Cyp1a1. Our findings underscore miR-96’s essential role in adult hearing maintenance and NIHL prevention, presenting it as a promising therapeutic target.

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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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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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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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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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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.

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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.

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Project description:To investigate the early changes in the hippocampus following noise-induced hearing loss, the gene expression profile of the hippocampus was evaluated using microarray analyses immediately after exposure to intense noise stimuli.

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

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