Ontology highlight
ABSTRACT:
PROVIDER: PRJNA941029 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23825904_1.fastq.gz | Fastqsanger.gz | |||
| SRR23825904_2.fastq.gz | Fastqsanger.gz | |||
| SRR23825905_1.fastq.gz | Fastqsanger.gz | |||
| SRR23825905_2.fastq.gz | Fastqsanger.gz | |||
| SRR23825906_1.fastq.gz | Fastqsanger.gz |
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Project description:Age-related hearing loss (ARHL) is involved in the hair cell apoptosis, but the underlying mechanism of hair cell apoptosis remains unclear. Here, we explored expression profiles of lncRNAs and mRNAs in an ARHL mouse model by using RNA sequencing and found that the cell apoptosis signaling pathway was activated in the cochlea tissues of old mice compared with those of young mice. We further found that lncRNA Mirg was most correlated with the cell apoptosis signaling pathway by the coexpression analysis. LncRNA Mirg was increased in the cochlea tissues of old mice compared with those of young mice, and its overexpression promoted hair cell apoptosis. H2O2-induced oxidative stress increased hair cell apoptosis by upregulating lncRNA Mirg. Furthermore, the expression of lncRNA Mirg and Foxp1 had the maximal correlation coefficient in the cochlea tissues of old mice, and lncRNA Mirg promoted hair cell apoptosis by increasing Foxp1 expression. In conclusion, we identified that oxidative stress-induced lncRNA Mirg promoted hair cell apoptosis via increasing Foxp1 expression, and these suggest that the lncRNA Mirg/Foxp1 signal may be a potential therapeutic target for ARHL.
2023-06-06 | GSE233798 | GEO
Project description:Through the intervention of traditional Chinese medicine prescription on cochlear hair cell apoptosis of c57 mice to 7-month-old mice, the proteomic analysis of cochlear hair cell apoptosis of 7-month-old mice and 2-month-old mice in the non traditional Chinese medicine group was compared to try to find the target or related pathway of Chinese medicine affecting cochlear senile apoptosis.
2023-05-04 | PXD041998 |
Project description:Cochlear hair cells are the sensory cells responsible for transduction of acoustic signals. In mammals, damaged hair cells do not regenerate, resulting in permanent hearing loss. Reprogramming of the surrounding supporting cells to functional hair cells represent a novel strategy to hearing restoration. However, cellular processes governing the efficient and functional hair cell reprogramming are not completely understood. Employing the mouse cochlear organoid system, we performed detailed metabolomic characterizations of the expanding and differentiating organoids. We found that hair cell differentiation is associated with increased mitochondrial electron transport chain (ETC) activity and reactive oxidative species generation. Transcriptome and metabolome analyses indicate reduced expression of oxidoreductases and tricyclic acid (TCA) cycle metabolites. The metabolic decoupling between ETC and TCA cycle limits the availability of the key metabolic cofactors, α-ketoglutarate and NAD+. Reduced expression of NAD+ in cochlear supporting cells by PGC1α deficiency further impairs hair cell reprogramming, while supplementation of α-ketoglutarate and NAD+ promotes hair cell reprogramming both in vitro and in vivo. Our findings reveal metabolic rewiring as a central cellular process during hair cell differentiation, and highlight the insufficiency of key metabolites as a metabolic barrier for efficient hair cell reprogramming.
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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.
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Project description:This study examined transcripts that are enriched in neonatal mouse cochlear hair cells. Hair cells were purified by FACS sorting for GFP fluorescence from the cochleas of transgenic mice in which the endogenous Atoh1 gene was fused with GFP Two replicates of GFP+ hair cells were compared with all other cochlear cell types that were GFP-
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Project description:The homeobox transcription factor Prox1 is critical for organogenesis including brain, retina, liver and pancreas and lymphatic system. Prox1 is transiently expressed in mouse cochlear hair cells (HCs) and supporting cells (SCs), however, it remains elusive about its in vivo DNA binding site and roles during cochlear development. Here, by using fresh cochlear tissues and Prox1 antibody, we firstly mapped out the genome-wide binding sites of Prox1 via Cleavage Under Targets and Release Using Nuclease (CUT&RUN). Gene function enrichment analysis suggests several potential functions of Prox1, one of which is regulating cell cycle progression. Secondly, to validate our CUT&RUN data, we further performed in vivo prox1 gain-of-function studies through genetic approaches. Onset of ectopic Prox1 at early embryonic otocyst leads to shorter cochlea with density of HCs and SCs distribution, suggesting a precocious cell cycle exit of cochlear sensory progenitor cells. These findings highlight the power of CUT&RUN in mapping DNA binding sites even in tissues (i.e. cochlea) with rare cells, as well as providing the first genetic evidence to support roles of Prox1 in regulating progenitor pools of cochlear progenitors.
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Project description:A balance of morphogen gradients during embryogenesis is thought to determine the identity of inner ear end organs. We applied this developmental principle to aggregates of human pluripotent stem cells and found that modulations of Sonic Hedgehog and WNT signaling promote stem cell-derived otic progenitors to express ventral otic markers. Strikingly, these ventralized otic progenitors gave rise to hair cells with short hair bundles comprised of stereocilia arrayed in a geometry reminiscent of cochlear hair cells. Moreover, these ventralized hair cells expressed multiple markers defining outer or inner hair cells in the cochlea. These results reveal that early morphogenic signals are sufficient for not only establishing cochlear gene expression, but also defining structural properties pertaining to the cochlear sensory epithelium.
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Project description:Effect of RG108 on cisplatin-induced apoptosis of cochlear hair cells
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Project description:Juvenile and mature mouse cochleae contain various low-abundant, vulnerable sensory epithelial cells embedded in the calcified temporal bone, making it challenging to profile the dynamic transcriptome changes of these cells during maturation at the single-cell level. Here we performed the 10X Genomics single-cell RNA sequencing (scRNA-seq) of mouse cochleae at postnatal days 14 (P14) and 28. We attained the transcriptomes of multiple cell types, including hair cells, supporting cells, spiral ganglia, stria fibrocytes, and immune cells. Our hair cell datasets are consistent with published transcripts from bulk RNA seq and scRNA-seq. We also mapped known deafness genes to corresponding cochlear cell types. Importantly, pseudotime trajectory analysis revealed that inner hair cells peak their maturation at P14 while outer hair cells continue to develop until P28. We further identified and confirmed a long noncoding RNA gene Miat expressed during maturation in cochlear hair cells and spiral ganglia neurons. Our transcriptomes of juvenile and mature mouse cochlear cells provided the sequel to those previously published at late embryonic and early postnatal ages and will be valuable resources to investigate cochlear maturation at single-cell resolution.
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