Analysis of the gene expression within the cochlea of aging C57BL6j mice.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE35234 | GEO | 2012/01/21
SECONDARY ACCESSION(S): PRJNA152749
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression within the cochlea of C57BL6j mice was examined. The hypothesis was that there was a genetic component to Age Related Hearing Loss and microarray would be useful in detecting candidate genes. Mice were aged in the laboratory to 4, 15 and 45 weeks of age. The cochlea were removed and pooled into groups of 5 for each age group. Total RNA was extracted and used in the micoroarray analysis. Differential expression was analysed between the different age groups i.e 4 - 15, 4 - 45 and 15 - 45 weeks.
2012-01-21 | E-GEOD-35234 | biostudies-arrayexpress
Project description:Our work describes the application of mass spectrometry-based label-free quantitative proteomics for the identification of differentially expressed proteins between different-aged cochlea. We report proteins exclusively present as well as up- and downregulated in the cochlear sensory epithelium at significant developmental stages. Additionally, we report proteins exclusively present on P3 that were recently identified in the cochlea for the first time. We use bioinformatics to provide insight on biological functions and potential primary and secondary partners of the differentially expressed proteins. This study provides the first differentially expressed proteome in the mammalian cochlea at significant developmental stages; before hearing, during the onset of hearing, and when hearing is fully developed. We believe that these results will provide insights into the function of proteins that change during development and identify potential protein biomarkers related to hearing impairments.
2018-08-29 | PXD001973 | Pride
Project description:To identify which miRNAs are involved in the onset and progression of age-related hearing loss in the mammalian cochlea We used miRNA microarrays to screen the miRNAs which exhibit the drastic changes in their expressing level during the aging of the cochlea The organ of Corti (OC), the major pathological sites of presbycusis in cochlea, was collected separately at 3 timepoints during the life span. Two strains were selected: C57bl/6j (as accelerated prebycusis model) and CBA/J (as naturally occured presbycusis model). The selected timepoints were: Postnatal 21 days (P21), 3 month (3m) and 9 month (9m) for C57 mice, and P21, 9m, 16m for CBA mice.
2013-03-12 | E-GEOD-45026 | biostudies-arrayexpress
Project description:Age-related hearing loss (AHL) is the progressive loss of auditory function with aging. The DBA/2J (DBA) mice have been used as a model of AHL and undergoes progressive, age-related hearing loss by 12 weeks of age. Here we analyzed cochlear gene expression of 7-week-old and 36-week-old DBA mice using microarrays. Auditory brainstem response (ABR) analysis confrimed that severe age-related hearing loss occured in 36-week-old mice, whereas moderate hearing loss occured in 7-week-old mice. Comprehensive gene expression analysis identified genes correlated with AHL and revealeed that 15 mitochondrial process categories, including â??mitochondrial electron transport chainâ??, â??oxidative phosphorylationâ??, â??respiratory chain complex Iâ??, â??respiratory chain complex IVâ??, and â??respiratory chain complex Vâ??, were statistically associated with AHL-correlated genes in the cochlea of 36-week-old DBA mice, and that 25 genes encoding components of the mitochondrial respiratory chain (respiratory chain complex I, IV, and V) were significantly down-regulated in the cochlea. These observations provide evidence that AHL is associated with down-regulation of genes involved in the mitochondrial respiratory chain in the cochlea of DBA mice, and suggest that mitochondrial respiratory chain dysfunction may be a key feature of AHL in mammalian cochlea. Experiment Overall Design: To determine the effects of age-related hearing loss, each 7-week-old sample (n = 3) was compared to each 36-week-old sample (n = 3), generating a total of nine pairwise comparisons. Using DAVIS and EASE, the identified genes were assign to â??GO: Biological Processâ?? categories of Gene Ontology Consortium. Furthermore, we used EASE to determine the total number of genes that were assigned to each biological process category, and to perform Fisher exact test. Quality control measures were not used. No replicates were done. Dye swap was not used.
2008-06-14 | E-GEOD-6045 | biostudies-arrayexpress
Project description:Age-related hearing impairment (ARHI), one of the most common medical conditions, is strongly heritable, yet its genetic causes remain largely unknown. We conducted a meta-analysis of GWAS summary statistics from multiple hearing-related traits in the UK Biobank (n = up to 323,978) and identified 31 genome-wide significant risk loci for self-reported hearing difficulty (p < 5e-8), of which 30 have not been reported previously at genome-wide significance. We interpreted these loci in the context of newly generated ATAC-seq and single-cell RNA-seq from cells in the mouse cochlea. Risk-associated genes were enriched for expression in cochlear epithelial and non-epithelial cells, as well as for genes related to sensory perception and known Mendelian deafness genes, supporting their relevance to auditory function. Regions of the human genome homologous to open chromatin in sensory epithelial cells from the mouse were strongly enriched for heritable risk for hearing difficulty, even after adjusting for baseline effects of evolutionary conservation and cell-type non-specific regulatory regions. Epigenomic and statistical fine-mapping most strongly supported 50 putative risk genes. Of these, at least 45 were expressed in mouse cochlea and 15 were enriched specifically in sensory hair cells. These results reveal new risk loci and risk genes for hearing difficulty and suggest an important role for altered gene regulation in the cochlear sensory epithelium.
2020-08-01 | GSE135737 | GEO
Project description:Alzheimer's disease (AD) is the most common type of dementia and is characterized by cognitive and behavioral impairment that significantly interferes with social functioning. Over the last decade, there has been an increased interest in whether sensory deficiency may be associated with the development of AD. Notably, the relationship between hearing impairment and AD is of great relevance, but still poorly understood. In this study, we found an early-onset hearing loss in 3xTgAD and 3xTgAD/Polβ+/− mouse models. The hearing assessment was measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) recordings. Herein, we report that both 3xTgAD and 3xTgAD/Polβ+/− mice showed increased ABR thresholds between at 16 and 32 kHz at 4 weeks of age, much earlier than any AD behavioral changes. The ABR thresholds were significantly higher in 3xTgAD/Polβ+/− mice than in 3xTgAD mice at 16 kHz, and DPOAE signals were also reduced, indicating that DNA damage may affect hearing impairment in AD. Poly ADP-ribosylation levels and protein expression of DNA damage markers increased significantly and NAD+ levels were reduced in the cochlea of 3xTgAD and 3xTgAD/Polβ+/− mice. Remarkably, we observed the downregulation of phosphoglycerate mutase 2 (PGAM2) in cochlea and a decrease in the number of synaptic ribbons in the presynaptic zones of inner hair cells in 3xTgAD/Polβ+/− mice. We also find that the activity of sirtuin 3 (SIRT3) is downregulated in cochlea, indicative of impaired mitochondrial function. Taken together, hearing impairment may be a potential early marker of AD. In addition, these findings provide new insights into the mechanism of the relationship between hearing dysfunction and AD and suggest that DNA damage in the cochlea can contributes to the development of early hearing loss of AD. The hearing assessment was measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) at 4 weeks of age, thereafter whole cochlea and auditory cortex tissue were collected from each mouse (WT, Polβ+/−, 3xTgAD, and 3xTgAD/Polβ+/−) and subjected to total RNA isolation to understand what metabolism-related gene expression changes in cochlea and auditory cortex.
2024-03-27 | GSE232205 | GEO
Project description:Age-related hearing loss (AHL) is the progressive loss of auditory function with aging. The DBA/2J (DBA) mice have been used as a model of AHL and undergoes progressive, age-related hearing loss by 12 weeks of age. Here we analyzed cochlear gene expression of 7-week-old and 36-week-old DBA mice using microarrays. Auditory brainstem response (ABR) analysis confrimed that severe age-related hearing loss occured in 36-week-old mice, whereas moderate hearing loss occured in 7-week-old mice. Comprehensive gene expression analysis identified genes correlated with AHL and revealeed that 15 mitochondrial process categories, including “mitochondrial electron transport chain”, “oxidative phosphorylation”, “respiratory chain complex I”, “respiratory chain complex IV”, and “respiratory chain complex V”, were statistically associated with AHL-correlated genes in the cochlea of 36-week-old DBA mice, and that 25 genes encoding components of the mitochondrial respiratory chain (respiratory chain complex I, IV, and V) were significantly down-regulated in the cochlea. These observations provide evidence that AHL is associated with down-regulation of genes involved in the mitochondrial respiratory chain in the cochlea of DBA mice, and suggest that mitochondrial respiratory chain dysfunction may be a key feature of AHL in mammalian cochlea. Keywords: Disease state analysis, Time course analysis
2007-10-16 | GSE6045 | GEO
Project description:This study demonstrates the baseline data of gradient gene expression in the cochlea. Especially for genes whose mutations cause autosomal dominant non syndromic hearing loss (Pou4f3, Slc17a8, Tmc1, and Crym) as well as genes important for cochlear function (Emilin-2 and Tectb), gradual expression changes help to explain the various pathological conditions. Four C57BL/6 mice aged 6 weeks cochlea samples including the lateral wall, stria vascularis, spiral ligament, spiral prominence, and the organ of corti were dissected and separated into the apical, middle and basal turns to compare gene expression profiles of each cochlea turn.
2014-01-08 | E-GEOD-53863 | biostudies-arrayexpress
Project description:Treatment of DBA/2J mice with a combination of L-methionine and valproic acid significantly attenuated progressive hearing loss. We examined gene expression in the whole cochlea of the mice. This study was aimed to detect genes of which change in expression levels were associated with attenuation of progressive hearing loss in the mice.
2015-04-15 | GSE62173 | GEO
Project description:Treatment of DBA/2J mice with a combination of L-methionine and valproic acid significantly attenuated progressive hearing loss. We examined gene expression in the whole cochlea of the mice. This study was aimed to detect genes of which change in expression levels were associated with attenuation of progressive hearing loss in the mice. DBA/2J mice at 4 weeks old (untreated_4-weeks, N=5), mice treated with control vehicle (0.1M sodium bicarbonate) for 8 weeks (Control_vehicle_12-weeks, N=5), and mice treated with L-methionine and valproic acid (MET_and_VA_12-weeks, N=6) were analyzed.
2015-04-15 | E-GEOD-62173 | biostudies-arrayexpress