Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Potential roles for lncRNA Mirg/Foxp1 in an ARHL model created using C57BL/6J mice hearing research

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE233798 | GEO | 2023/06/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:LncRNA Mirg promotes cochlear hair cell apoptosis by regulating Foxp1 in ARHL

| PRJNA941029 | ENA

Molecular changes associated with biological aging of cochlear hair cells

Project description:Age-related hearing loss (ARHL) is a progressive sensorineural hearing loss that occurs as people get older. As many as 35% to 50% of the population aged between 65 and 75 have ARHL. Although age-related changes in the central auditory system can contribute to hearing impairment, degeneration of the mechanosensitive hair cells in the cochlea is the prevalent cause of ARHL. The molecular mechanisms of hair cell aging are largely unknown. To provide a comprehensive dataset of age-related genes and pathways in hair cells, we individually collected inner and outer hair cells, the two types of sensory receptor cells in the cochlea, from 9- and 26-month-old CBA/J mice and performed cell type-specific transcriptomic analysis. Our analysis showed a significant reduction of the expression of genes related to hair cell structure and function such as Tmc1, Kcnq4, Kcnj13, Slc7a14, Slc17a8, Chrna9/Chrna10, and Slc26a5. Our hair cell-specific transcriptome analysis provides a rich resource for mechanistic studies of biological aging of cochlear hair cells.

2022-03-01 | GSE153882 | GEO

scRNA-seq of P20 mouse cochlea

Project description:ARHL has been thought to result from disordered hair cell function and their loss. ARHL has a significant genetic component. We sought to determine the expression in the cochlea of genes associated with single nucleotide polymorphisms linked to ARHL. We find widespread and varying expression of genes associated with these SNPs in subtypes of cells in the cochlea identified by single-cell RNA sequencing. Genes associated with SNPs with the highest significance were preferentially expressed highly in hair cells while genes associated with SNPs with a lower significance were expressed more universally.

2021-08-05 | GSE181454 | GEO

The Study of Chinese Medicine Intervention on Apoptosis of Cochlear hair cells in C57BL/6J Aged Cochlea

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 |

Redox activation of excitatory pathways in auditory neurons as mechanism of age-related hearing loss

Project description:Age-related hearing (ARHL) loss affects a large part of the human population with a major impact on our aging societies. Yet, underlying mechanisms are not understood, and no validated therapy or prevention exists. NADPH oxidases (NOX), are important sources of reactive oxygen species (ROS) in the cochlea and might therefore be involved in the pathogenesis of ARHL. Here we investigate ARHL in a mouse model. Wild type mice showed early loss of hearing and cochlear integrity, while animals deficient in the NOX subunit p22phox remained unaffected up to six months. Genes of the excitatory pathway were down-regulated in p22phox-deficient auditory neurons. Our results demonstrate that NOX activity leads to upregulation of genes of the excitatory pathway, to excitotoxic cochlear damage, and ultimately to ARHL. In the absence of functional NOXs, aging mice conserve hearing and cochlear morphology. Our study offers new insights into pathomechanisms and future therapeutic targets of ARHL.

2020-12-18 | E-MTAB-8668 | biostudies-arrayexpress

Gene expression profiling of miR-183/96 knock out mouse cochlea

Project description:Transcriptome analysis of P16 cochlea from wild type and miR-183/96 Knock out mice Gene expression analysis of miR-183/96 KO cochlea revealed a set of hair cell-relevant differentially expressed genes that could adversely impact hair cell physiology and contribute to the observed phenotype.

2018-05-01 | GSE106599 | GEO

Long-term NAD+ supplementation prevents the progression of age-related hearing loss in mice

Project description:Age-related hearing loss (ARHL) is the most common sensory disabling condition associated with aging in humans. Yet, there are still no approved measures for preventing or treating this debilitating condition. With its slow progression, continuous and safe treatment approaches are critical for ARHL treatment. Nicotinamide Riboside (NR), a NAD+ precursor, is well-tolerated even for long-term use and is already shown effective in various disease models including Alzheimer’s and Parkinson’s Disease. However, its beneficial impact on ARHL is not known. In this study, we investigated transcriptomic profile in the cochlea of the mice (mtKeima strain) that are treated with NR for 10 months vs. non-treated.

2023-09-20 | GSE213994 | GEO

Mass spectrometry identification of proteins of isolated auditory and vestibular hair cells using data-independent and data-dependent acquisition

Project description:Hair cells undergo postnatal development that leads to formation of their sensory organelles, synaptic machinery, and in the case of cochlear outer hair cells, their electromotile mechanism. To examine the proteome changes over development, we isolated pools of 5000 Pou4f3-Gfp positive or negative cells from the cochlea or utricles; these cell pools were analyzed by data-dependent and data-independent acquisition (DDA and DIA) mass spectrometry. DDA data were used to generate spectral libraries, which enabled identification and accurate quantitation of specific proteins using the DIA datasets. We also isolated and pooled individual inner and outer hair cells from adult cochlea and compared their proteomes to those of developing hair cells. The DDA and DIA datasets will be valuable for accurately quantifying proteins in hair cells and non-hair cells over this developmental window.

2017-09-18 | PXD006240 | Pride

Transcription profiling of cochleae from young and middle aged mice subjected to calorie restriction to examine age-related changes and calorie restriction-induced changes in gene expression in the cochlea.

Project description:Presbycusis is characterized by an age-related progressive decline of auditory function, and arises mainly from the degeneration of hair cells or spiral ganglion (SG) cells in the cochlea. Here we show that caloric restriction suppresses apoptotic cell death in the mouse cochlea and prevents late onset of presbycusis. Caloric restricted mice, which maintained body weight at the same level as that of young control (YC) mice, retained normal hearing and showed no cochlear degeneration. CR mice also showed significantly fewer TUNEL-positive staining cells and fewer cleaved caspase-3-positive staining cells relative to middle-age control (MC) mice. Microarray analysis revealed that CR down-regulated the expression of 28 proapoptotic genes, including Bak and Bim. Taken together, our findings suggest that loss of critical cells through apoptosis is an important mechanism of presbycusis in mammals, and that CR or staying lean can retard this process by suppressing apoptosis in the inner ear tissue. Experiment Overall Design: To examine the effects of aging, a comparison of cochlea tissues from YC (3 samples) and MC (3 samples) mice was conducted. To examine the effects of calorie restriction (CR), a comparison of cochleae from MC (3 samples) and CR (3 samples) mice was conducted. We examined age-related changes in gene expression in the cochlea and calorie restriction-induced changes in gene expression in the cochlea. We pooled four cochleae from two mice for one sample and used three samples per group (n = 3). Quality control measures were not used. No replicates were done. Dye swap was not used.

2007-11-22 | E-GEOD-4786 | biostudies-arrayexpress

Potential role of Bcl2 in lipid metabolism and synaptic dysfunction of age-related hearing loss

Project description:Age-related hearing loss (ARHL) is a prevalent disease that affects millions of people worldwide. BCL-2 gene plays a tremendous role in cellular senescence, and it was confirmed that the BCL-2 family is closely associated with neurological disorders and ARHL. In addition to modulating apoptosis and oxidative stress, as well as other effects, this study we report here that BCL-2 plays a crucial position in regulating phospholipid and lipid metabolism in the developing cochlear tissues of rats and a sensory epithelial cell line(OC1), including the cholesterol synthesis pathway that is differentially expressed by genes such as LSS,NSDHL, and CYP51, which further demonstrates the mechanism of the action of BCL-2 in hair cells. In conclusion our data provide a new molecular framework for the regulatory mechanism of BCL-2 down-regulation in senescent cells. These findings provide valuable insights into the molecular mechanisms of ARHL and may set the stage for new therapeutic approaches for this prevalent age-related disease.

2023-09-12 | GSE242359 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data