Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA330968 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Various organ failure induced by chronic intake of GeO2 is one of the well known disease related to mitochondrial dysfunction. The 0.15% GeO2 treated CBA mice shows severe hearing loss in 4M. Here we analyzed cochlear gene expression of 6 months old CBA mice using microarrays treated with normal chow or that containing 0.15% GeO2 for four months. Auditory brainstem response (ABR) analysis confirmed that severe age-related hearing loss occured in GeO2 treated mice, whereas no hearing loss occured in normal chow treated mice. Comprehensive gene expression analysis identified genes correlated with GeO2-induced mithochodrial dysfunction genes and revealed that 28 genes encoding components of the mitochondrial respiratory chain were significantly down-regulated. These observations provide evidence that GeO2-induced hearing loss is associated with the down-regulation of genes involved in the mitochondrial respiratory chain complexes in the cochlea of CBA mice.
2016-07-22 | GSE84735 | GEO
Project description:Transcriptome in mice cochlea with age related hearing loss
| PRJNA600057 | ENA
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
Project description:Gene expression profile of the age-related hearing loss cochlea in DBA/2J mice
| PRJNA97781 | ENA
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:Various organ failure induced by chronic intake of GeO2 is one of the well known disease related to mitochondrial dysfunction. The 0.15% GeO2 treated CBA mice shows severe hearing loss in 4M. Here we analyzed cochlear gene expression of 6 months old CBA mice using microarrays treated with normal chow or that containing 0.15% GeO2 for four months. Auditory brainstem response (ABR) analysis confirmed that severe age-related hearing loss occured in GeO2 treated mice, whereas no hearing loss occured in normal chow treated mice. Comprehensive gene expression analysis identified genes correlated with GeO2-induced mithochodrial dysfunction genes and revealed that 28 genes encoding components of the mitochondrial respiratory chain were significantly down-regulated. These observations provide evidence that GeO2-induced hearing loss is associated with the down-regulation of genes involved in the mitochondrial respiratory chain complexes in the cochlea of CBA mice. To determine the effects of GeO2, each control sample (n=5) was compared to each GeO2-intoxicated (n=5), generating a total of 25 pairwise comparisons. Using DAVIS and EASE, the identified genes were assign to GO: Biological Process 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.
2016-07-22 | E-GEOD-84735 | biostudies-arrayexpress
Project description:Presbycusis – age-related hearing loss – is the number one communicative disorder of our aged population. Here we analyzed gene expression for a set of GABA receptors in the cochlea of aging CBA mice using the Affymetrix GeneChip MOE430A. Functional phenotypic hearing measures distortion-product otoacoustic emission (DPOAE) amplitudes (four age groups) were made. The gene expression changes from RMA normalized microarray data (40 replicates) were first subjected to one-way ANOVA, and then linear regression was performed. In addition, the log signal ratio was converted to fold change, and selected gene expression changes were confirmed by relative real-time PCR. Major findings: expression of GABA-A receptor subunit 6was upregulated with age and hearing loss, whereas subunit 1 was repressed. In addition, GABA-A receptor associated protein like-1 and GABA-A receptor associated protein like-2 were strongly downregulated with age and hearing impairment. Lastly, gene expression measures were correlated with pathway/network relationships relevant to the inner ear using Pathway Architect, to identify key pathways consistent with the gene expression changes observed. In the study of expression changes GABA receptors in the in cochlea of young adult and aging presbycusis mice total of forty chips were used. The normal aging mice were in four groups young adults controls with good hearing (8 mice, 8 MOE430A GeneChips), Middle aged group with good hearing ( 17 mice, 17 MOE430A GeneChips), Mild Presbycusis (old) with limited hearing loss (9 mice, 9 MOE430A GeneChips) and Severe Presbycusis (old) (6 mice, 6 MOE430A GeneChips). Each Mice cochlea to each GeneChips, Samples was not pooled. The hearing potential evidence of each mouse is accompanied with each mice DPOAE amplitude.
2013-08-06 | E-GEOD-49543 | biostudies-arrayexpress
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
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