MicroRNA Expression of Mouse Cochleae during Aging
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ABSTRACT:
ORGANISM(S): synthetic construct Mus musculus
PROVIDER: GSE45026 | GEO | 2013/03/12
SECONDARY ACCESSION(S): PRJNA192856
REPOSITORIES: GEO
Similar Datasets
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: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: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: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
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 is a progressive sensorineural hearing loss that occurs as people get older. Degeneration of the organ of Corti and atrophy of the lateral wall of the cochlear duct (or scala media) in the inner ear are the two primary causes. MicroRNAs (miRNAs), a class of short non-coding RNAs that regulate the expression of mRNA/protein targets, are important regulators of cellular senescence and aging. We examined the change of miRNA gene expression profiles in the lateral wall of the cochlear duct in two mouse strains during aging The totoal RNA was extracted from the lateral wall of cochlear duct from CBA/J and C57BL/6J mice at different ages. The expression profile of miRNAs was examined by miR microarray GeneChip.
2014-10-01 | E-GEOD-57782 | biostudies-arrayexpress
Project description:The Gfi1-Cre mouse is commonly used for conditional hair cell-specific gene deletion/activation in the inner ear. However, we have shown that these mice produce a pattern of recombination that is not strictly limited to hair cells, and that Gfi1cre/+ mice exhibit an early onset progressive hearing loss as compared with their wildtype littermates. Here we performed a transcriptome analysis of Gfi1cre/+ and Gfi1+/+ cochlea to detect potential changes in gene expression that could contribute to their hearing loss phenotype, or that could potentially confound downstream analysis of conditional gene deletion using these mice.
2017-03-09 | GSE85519 | GEO
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:Age-related hearing loss is a progressive sensorineural hearing loss that occurs as people get older. Degeneration of the organ of Corti and atrophy of the lateral wall of the cochlear duct (or scala media) in the inner ear are the two primary causes. MicroRNAs (miRNAs), a class of short non-coding RNAs that regulate the expression of mRNA/protein targets, are important regulators of cellular senescence and aging. We examined the change of miRNA gene expression profiles in the lateral wall of the cochlear duct in two mouse strains during aging
2014-10-01 | GSE57782 | GEO
Project description:The critical role of the endothelium in governing vascular, tissues homeostasis and pathological processes is increasingly recognized (Deanfield et al., 2007). Cellular senescence of endothelial cells has been proposed to be involved in endothelial dysfunction and atherogenesis (Minamino T et al., 2007), although the mechanisms underlying the aging induced attenuation of endothelium dependent functions are yet to be clarified. Recent evidences implicated overall miRNA levels and miRNA in regulating angiogenesis and endothelial function (Suarez et al., 2007; Kuehbacher et al., 2007; Harris et al., 2008; Fish et al. 2008; Wang et al., 2008). To investigate the role of miRNAs in endothelial cell senescence, we first profiled the miRNA signature during HUVECs aging (Maciag et al.,1981), through DNA microarray containing 200 oligonucleotide probes complementary to mature forms of miRNAs of human, mouse, and rat origin.
2010-06-25 | E-GEOD-14912 | biostudies-arrayexpress