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Single cell gene expression profile of adult cochlear in NIHL vs. ISL1-NIHL

ABSTRACT: Single cell gene expression profile of adult cochlear in NIHL vs. ISL1-NIHL

PROVIDER: PRJNA903156 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22334949_1.fastq.gz	Fastqsanger.gz
	SRR22334949_2.fastq.gz	Fastqsanger.gz
	SRR22334950_1.fastq.gz	Fastqsanger.gz
	SRR22334950_2.fastq.gz	Fastqsanger.gz

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Single cell gene expression profile of adult cochlear in NIHL vs. ISL1-NIHL

Project description:Exposure to excessive noise levels is considered one of the main etiologies of acquired hearing loss. Noise-induced hearing loss (NIHL) affects a large number of people during the productive years of life, and imposes a large impact on quality of life and a high socioeconomic burden. Here, we tested the effect of the ISL1 in NIHL. We used an inbred mouse strain (CBA/CaJ) and carried out single-cell RNA sequencing to examine the gene expression profiles comparing (AAV-ISL1) with (NIHL-only).

2023-06-01 | GSE218328 | GEO

Single cell gene expression profile of adult cochlear explants over the course of hair cell regeneration stimulated by Atoh1 activation [DoxVehicleAtoh1]

Project description:Strategies to overcome irreversible cochlear hair cell (HC) damage and loss are of vital importance to develop a treatment for hearing loss. HC regeneration in adult cochlea relies on a two-phase process: 1) Reprogramming mature cochlear (SCs) to regain the properties of their younger selves; 2) Activating Atoh1, a gene responsible for HC fate-determining, in the reprogrammed adult SCs for HC regeneration. We have shown that, by transient co-activation of Myc and NICD (Notch1 intracellular domain), the adult mouse cochlea can be successfully reprogrammed to a relatively younger stage and regain progenitor capacity, with the regeneration of HCs following Atoh1 overexpression in vitro and in vivo. To identify molecules to reprogram mature cochlear SCs and HC regeneration, we utilized single-cell RNA sequencing and uncovered the pathways and their target genes underlying MYC/NICD-mediated reprogramming. We used an in-house adult cochlea explant culture system and carried out single-cell RNA sequencing to examine the gene expression profiles of cochlear explants from a transgenic mouse model, rtTa/tet-Myc/-tet-NICD, in response to Dox-induced MYC/NICD co-activation. We compared gene expression profiles between Atoh1 activation vs. MYC/NICD/Atoh1 co-activation.

2023-06-01 | GSE218325 | GEO

Gene expression profile in the developing and adult mouse cochlear sensory epithelia

Project description:To understand the molecular control of development and regeneration in the mammalian cochlear sensory epithelia, we performed a comparative study of gene expression patterns between postnatal day-3 (P3) and adult stages using a microarrays approach. Two inner ear development stages were used in this study, Post-natal day three and eight-week-old adult. A total number of sixty Swiss mice were exploited for each stage. The cochlear sensory epithelia (CSE) were collected from the inner ears and immediately placed in RNA later solution. A total of six independent dissection experiments were carried out separately in order to obtain three biological replicates for each stage. In each experiment, the CSE from 20 mice were pooled. Total RNA was purified from each biological sample separately using RNAeasy Mini Kit and the RNA integrity was assessed by the Nanodrop 2000

2012-01-01 | E-GEOD-32963 | biostudies-arrayexpress

Single cell gene expression profile of adult cochlear explants over the course of hair cell regeneration stimulated by chemical reprogramming [CocktailVehicleAtoh1]

Project description:Strategies to overcome irreversible cochlear hair cell (HC) damage and loss are of vital importance to develop a treatment for hearing loss. HC regeneration in adult cochlea relies on a two-phase process: 1) Reprogramming mature cochlear (SCs) to regain the properties of their younger selves; 2) Activating Atoh1, a gene responsible for HC fate-determining, in the reprogrammed adult SCs for HC regeneration. We have shown that, by transient co-activation of Myc and NICD (Notch1 intracellular domain), the adult mouse cochlea can be successfully reprogrammed to a relatively younger stage and regain progenitor capacity, with the regeneration of HCs following Atoh1 overexpression in vitro and in vivo. We identified a combination (the cocktail) of drug-like molecules composing of small molecules and siRNAs to activate the pathways of Myc, Notch1, Wnt and cAMP. To identify molecules to reprogram mature cochlear SCs and HC regeneration, we utilized single-cell RNA sequencing and uncovered the pathways and their target genes underlying chemical-mediated reprogramming. We used an in-house adult cochlea explant culture system and carried out single-cell RNA sequencing to examine the gene expression profiles of cochlear explants, in response to chemical-induced reprogramming. We compared gene expression profiles between Vehicle/ad.Atoh1 activation vs. Cocktail (chemical reprogramming)/ad.Atoh1 activation.

2023-06-01 | GSE218324 | GEO

Gene expression profile in the developing and adult mouse cochlear sensory epithelia

2012-01-01 | GSE32963 | GEO

Identification of intermediate transcriptome states and synergistic effects of Isl1 in Atoh1-mediated cochlear hair cell conversion

Project description:Ectopic expression of Atoh1 in non-sensory supporting cells (SCs) in mouse cochleae induces their conversion to hair cells (HCs) in vivo. cHCs in multiple intermediate states of the conversion process that most closely resembled neonatal differentiating HCs, but differed from the progenitors. We further identified 52 transcription factors that are differentially expressed in cHCs, SCs, and mature HCs and confirmed that Isl1 synergistically enhanced the efficiency of Atoh1-mediated HC conversion in cochlear explants. Our results demonstrate that direct HC conversion from SCs in vivo follows a different path from normal development and requires multiple factors for maximum efficiency and completion.

2018-07-23 | GSE85983 | GEO

ISL1

Project description:ISL1

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ISL1 is an essential determinant of structural and functional tonotopic representation of sound

Project description:A cardinal feature of the auditory pathway is frequency selectivity represented in the form of a tonotopic map from the cochlea to the cortex. The molecular determinants of the auditory frequency map are unknown. Here, we discovered that the transcription factor ISL1 regulates features of auditory neurons, including the formation of the spiral ganglion neuron (SGN) and peripheral and central processes that shape the tonotopic representation of the auditory map. We selectively knocked out Isl1 in auditory neurons using Neurod1Cre strategies. In the absence of Isl1, SGNs migrate into the central cochlea and beyond. The cochlear wiring is profoundly reduced and disrupted. The central axons of Isl1 mutants lose their topographic projections and segregation at the cochlear nucleus. Transcriptome analysis of SGNs shows that Isl1 regulates neurogenesis, axonogenesis, migration, and the functional properties of neurons. Surprisingly, notable auditory processing features are preserved despite the significant hearing impairment, revealing central auditory pathway resilience and plasticity in mutant mice. Mutant mice demonstrate altered acoustic startle reflex, prepulse inhibition, characteristics of compensatory neural hyperactivity centrally. Our findings show that the Isl1 is one of the obligatory factors required to sculpt auditory structural and functional tonotopic maps. Still, upon Isl1 deletion, the ensuing compensatory plasticity of the auditory pathway does not suffice to overcome developmental changes at the peripheral sensory organ.

2022-09-01 | GSE182575 | GEO

Characterizing adult cochlear supporting cell transcriptional diversity using single-cell RNA-Seq: Validation in the adult mouse and translational implications for the adult human cochlea

Project description:Characterizing adult cochlear supporting cell transcriptional diversity using scRNA-Seq Hearing loss is a significant disability that impacts 432 million people worldwide. A significant proportion of these individuals are dissatisfied with or do not have access to available treatment options which include hearing aids and cochlear implants. An alternative approach to restore hearing would be to regenerate lost cells, including hair cells in the adult cochlea. Such therapy would require restoration of the organ of Corti’s complex architecture, necessitating regeneration of both mature hair cells and supporting cells. We characterize the first single-cell adult cochlear supporting cell transcriptomes with the goals of: (1) demonstrating their transcriptional distinctiveness from perinatal cochlear supporting cells, (2) providing a metric for future attempts at regenerating mature cochlear supporting cells by identifying both cell type-specific and regional-specific expression, and (3) identify cell cycle gene expression present in adult supporting cells at the single cell level which may establish a basis for targeting cell cycle regulation pathways to force these cells out of quiescence.

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Unraveling the Molecular Landscape of Lead-Induced Cochlear Synaptopathy: A Quantitative Proteomic Analysis

Project description:This study investigates how lead exposure triggers cochlear synaptopathy and hearing loss in mice. Young-adult CBA/J mice were given lead acetate in drinking water for 28 days. We assessed hearing thresholds, outer hair cell activity, and synaptic changes in the cochlea. Lead exposure raises hearing thresholds, indicating cochlear synaptopathy. Notably affects synapses in the basal turn without impacting outer hair cells. In addition to this, lead altered the abundance of 352 synaptic proteins, with the synaptic vesicle cycle pathway prominently affected. Lead-induced cochlear synaptopathy targets basal cochlear regions, implicating synaptic vesicle cycle signaling in hearing loss. Revealing specific mechanisms behind lead-induced hearing deficits enhances targeted interventions and preventive strategies, advancing our understanding of lead induced hearing loss.

2024-10-17 | PXD050415 | Pride

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