Expression data of mRNA from normal utricle and vestibular flat epithelium of adult mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA742039 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The vestibular sensory epithelium may degenerate into a layer of flat cells, known as flat epithelium, after a severe lesion, but the pathogenesis of vestibular flat epithelium remains unclear. We used microarrays to detail the global programme of gene expression in normal utricle and vestibular flat epithelium and identified whether epithelial-mesenchymal transition participite in this process
2021-09-30 | GSE179063 | GEO
Project description:The avian utricle, a vestibular organ of the inner ear, displays turnover of sensory hair cells throughout life. This is in sharp contrast to the mammalian utricle, which shows limited regenerative capacity. Here, we use single-cell RNA-sequencing to identify distinct marker genes for the different sensory hair cell subtypes of the chicken utricle, which we validated in situ . We provide markers for spatially distinct supporting cell populations, and identified two transitional cell populations of dedifferentiating supporting cells and developing hair cells. Trajectory reconstruction resulted in an inventory of gene expression dynamics of natural hair cell generation in the avian utricle.
2022-09-07 | GSE212831 | GEO
Project description:Inner ear auditory and vestibular tissues differ in their responses to mechanical stimuli. Chick cochlea and utricle sensory epithelia were microdissected at E20-E21. RNA was extracted and cRNA hybridized to Affymetrix microarrays.
2012-01-01 | E-GEOD-32272 | biostudies-arrayexpress
Project description:Several compounds cause auditory and vestibular toxicity by targeting the sensory transducing cells of the inner ear, the hair cells (HC). These compounds, known as ototoxic compounds, may cause vestibular HC apoptosis following high dose acute exposure. However, chronic exposure to low doses has been observed to cause progressive damage. Thus, chronic ototoxic stress first cause detachment and uncoupling of the HC and their post-synaptic neurons, followed by changes in cell shape including stereocilia fusion and ending with extrusion of the HCs from the sensory epithelium towards the luminal spaces of the vestibule. The molecular mechanisms driving these phenomena have not been established. We hypothesized that this response of the vestibular epithelium to chronic ototoxic stress must include specific gene expression responses. The present SubSeries is part of a SuperSeries aimed at identifying these expression responses. Two species, two ototoxic compounds and different times were studied as a strategy to identify the most relevant responses. In the present SubSeries, the expression response of the vestibular epithelium is studied in rats exposed to streptomycin.
2025-09-10 | GSE292473 | GEO
Project description:Several compounds cause auditory and vestibular toxicity by targeting the sensory transducing cells of the inner ear, the hair cells (HC). These compounds, known as ototoxic compounds, may cause vestibular HC apoptosis following high dose acute exposure. However, chronic exposure to low doses has been observed to cause progressive damage. Thus, chronic ototoxic stress first cause detachment and uncoupling of the HC and their post-synaptic neurons, followed by changes in cell shape including stereocilia fusion and ending with extrusion of the HCs from the sensory epithelium towards the luminal spaces of the vestibule. The molecular mechanisms driving these phenomena have not been established. We hypothesized that this response of the vestibular epithelium to chronic ototoxic stress must include specific gene expression responses. The present SubSeries is part of a SuperSeries aimed at identifying these expression responses. Two species, two ototoxic compounds and different times were studied as a strategy to identify the most relevant responses. In the present SubSeries, the expression response of the vestibular epithelium is studied in mice exposed to 3,3'-iminodipropionitrile (IDPN).
2025-09-10 | GSE292468 | GEO
Project description:Several compounds cause auditory and vestibular toxicity by targeting the sensory transducing cells of the inner ear, the hair cells (HC). These compounds, known as ototoxic compounds, may cause vestibular HC apoptosis following high dose acute exposure. However, chronic exposure to low doses has been observed to cause progressive damage. Thus, chronic ototoxic stress first cause detachment and uncoupling of the HC and their post-synaptic neurons, followed by changes in cell shape including stereocilia fusion and ending with extrusion of the HCs from the sensory epithelium towards the luminal spaces of the vestibule. The molecular mechanisms driving these phenomena have not been established. We hypothesized that this response of the vestibular epithelium to chronic ototoxic stress must include specific gene expression responses. The present SubSeries is part of a SuperSeries aimed at identifying these expression responses. Two species, two ototoxic compounds and different times were studied as a strategy to identify the most relevant responses. In the present SubSeries, the expression response of the vestibular epithelium is studied in rats exposed to 3,3'-iminodipropionitrile (IDPN) for 4 weeks.
2025-09-10 | GSE292470 | GEO
Project description:Effect of subchronic ototoxic exposure on the vestibular epithelium
| PRJNA1238827 | ENA
Project description:Several compounds cause auditory and vestibular toxicity by targeting the sensory transducing cells of the inner ear, the hair cells (HC). These compounds, known as ototoxic compounds, may cause vestibular HC apoptosis following high dose acute exposure. However, chronic exposure to low doses has been observed to cause progressive damage. Thus, chronic ototoxic stress first cause detachment and uncoupling of the HC and their post-synaptic neurons, followed by changes in cell shape including stereocilia fusion and ending with extrusion of the HCs from the sensory epithelium towards the luminal spaces of the vestibule. The molecular mechanisms driving these phenomena have not been established. We hypothesized that this response of the vestibular epithelium to chronic ototoxic stress must include specific gene expression responses. The present SubSeries is part of a SuperSeries aimed at identifying these expression responses. Two species, two ototoxic compounds and different times were studied as a strategy to identify the most relevant responses. In the present SubSeries, the expression response of the vestibular epithelium is studied in rats exposed to 3,3'-iminodipropionitrile (IDPN) for 3 or 7 weeks.
2025-09-10 | GSE292500 | GEO
Project description:The mammalian cochlea loses its ability to regenerate new hair cells prior to the onset of hearing. In contrast, the adult vestibular system can produce new hair cells in response to damage, or by reprogramming of supporting cells with the hair cell transcription factor Atoh1. We used RNA-seq and ATAC-seq to probe the transcriptional and epigenetic responses of utricle supporting cells to damage and Atoh1 transduction. We show that the improved regenerative response of the utricle correlates with a more accessible chromatin structure in utricle supporting cells compared to their cochlear counterparts. We also provide evidence that Atoh1 transduction of supporting cells is able to promote increased transcriptional accessibility of some hair cell genes. Our study offers a possible explanation for regenerative differences between sensory organs of the inner ear, but shows that additional factors to Atoh1 may be required for optimal reprogramming of hair cell fate.
2019-04-30 | GSE121610 | GEO
Project description:Purified utricle hair bundles and utricular epithelium from P3-P7 rat inner ears were analyzed by LC-MS/MS to determine the abundant and enriched proteins of the hair bundle. This dataset used a Thermo LTQ mass spectrometer for protein detection.
2015-11-17 | PXD002416 | Pride