Impact of acute noise trauma on the gene expression profile of the hippocampus
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ABSTRACT:
PROVIDER: PRJNA588236 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To investigate the early changes in the hippocampus following noise-induced hearing loss, the gene expression profile of the hippocampus was evaluated using microarray analyses immediately after exposure to intense noise stimuli.
2020-10-17 | GSE140087 | GEO
Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss and dexamethasone therapy in the cochlea (inner ear), transcriptome of cochlear samples was analyzed after induction of hearing loss by exposure to intense noise in mice. Dexamethasone was intraperitoneally injected immediately following the noise trauma. Cochlear transcriptome was analyzed at 12h and 24h following the noise trauma and dexamethasone administration.
2016-12-03 | GSE85290 | GEO
Project description:Cochlear transcriptome at 3 hours post-noise trauma in mice
| PRJNA573471 | ENA
Project description:BackgroundThis study aimed to investigate the changes in the expression of hippocampal genes upon acute noise exposure.MethodsThree-week-old Sprague-Dawley rats were assigned to control (n = 15) and noise (n = 15) groups. White noise (2-20 kHz, 115 dB sound pressure level [SPL]) was delivered for 4 h per day for 3 days to the noise group. All rats were sacrificed on the last day of noise exposure, and gene expression in the hippocampus was analyzed using a microarray. Pathway analyses were conducted for genes that showed differential expression ≥ 1.5-fold and P ≤ 0.05 compared to the control group. The genes included in the putative pathways were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR).ResultsThirty-eight upregulated genes and 81 downregulated genes were identified. The pathway analyses revealed that upregulated genes were involved in the cellular responses to external stimuli and immune system pathways. qRT-PCR confirmed the upregulation of the involved genes. The downregulated genes were involved in neuronal systems and synapse-related pathways, and qRT-PCR confirmed the downregulation of the involved genes.ConclusionsAcute noise exposure upregulated the expression of immune-related genes and downregulated the expression of neurotransmission-related genes in the hippocampus.
| S-EPMC7648995 | biostudies-literature
Project description:In order to elucidate molecular mechanisms of noise-induced hearing loss in the cochlea (inner ear), transcriptome of the cochlear sample was analyzed after induction of hearing loss by exposure to intense noise in mice. Cochlear transcriptome was analyzed at 3 hours following the noise exposure.
2020-01-14 | GSE137817 | GEO
Project description:The cochlea possesses a robust circadian clock machinery that regulates auditory function. How the cochlear clock is influenced by the circadian system remains unknown. Here we show that cochlear rhythms are system-driven and require local Bmal1 as well as central input from the suprachiasmatic nuclei (SCN). SCN ablations disrupted the circadian expression of the core clock genes in the cochlea. Since the circadian secretion of glucocorticoids (GCs) is controlled by the SCN and that GCs are known to modulate auditory function, we assessed their influence on circadian gene expression. Removal of circulating GCs by adrenalectomy (ADX) did not have a major impact on core clock gene expression in the cochlea. Rather it abolished the transcription of clock-controlled genes involved in inflammation. ADX abolished the known differential auditory sensitivity to day and night noise trauma and prevented the induction of GABA-ergic and glutamate receptors mRNA transcripts. However, these improvements were unrelated to changes at the synaptic level suggesting other cochlear functions may be involved. Due to this circadian regulation of noise sensitivity by GCs, we evaluated the actions of the synthetic glucocorticoid dexamethasone (DEX) at different times of the day. DEX was effective in protecting from acute noise trauma only when administered during daytime, when circulating glucocorticoids are low, indicating that chronopharmacological approaches are important for obtaining optimal treatment strategies for hearing loss. GCs appear as a major regulator of the differential sensitivity to day or night noise trauma, a mechanism likely involving the circadian control of inflammatory responses.
2019-06-15 | GSE107086 | GEO
Project description:Environmental insults, including mild head trauma, significantly increase the risk of neurodegeneration. However, it remains challenging to establish a causative connection between early-life exposure to mild head trauma and late-life emergence of neurodegenerative deficits, nor do we know how sex and age compound the outcome. Using aDrosophilamodel, we demonstrate that exposure to mild head trauma causes neurodegenerative conditions that emerge late in life and disproportionately affect females. Increasing age-at-injury further exacerbates this effect in a sexually dimorphic manner. We further identify Sex Peptide (SP) signaling as a key factor in female susceptibility to post-injury brain deficits. RNA sequencing highlights changes in innate immune defense transcripts specifically in mated females during late life. Our findings establish a causal relationship between early head trauma and late-life neurodegeneration, emphasizing sex differences in injury response and the impact of age-at-injury. Finally, our findings reveal that reproductive signaling adversely impacts female response to mild head insults and elevates vulnerability to late-life neurodegeneration.
2024-08-29 | GSE274136 | GEO
Project description:Using the RiboTag approach, we profiled the cell type-specific molecular landscape of the outer hair cells and supporting cells as well as the whole cochlea, both before and after noise trauma (6h and 24h) that induces a permanent hearing loss.
2021-09-03 | GSE168973 | GEO
Project description:Toxoplasma gondii is a protozoan parasite with a remarkable neuro-tropismneurotropic affinity. We recently showed that T. gondii infection can alter the global metabolism of the cerebral cortex of the mice. However, the impact of this infection on the metabolism of the hippocampus remains unclear. In this study, we compared the metabolomic profiles of mouse hippocampus following acute and chronic infection with T. gondii. Our data provide new insight into the neuropathogenesis of T. gondii infection and reveal new pathways and metabolites that mediate the interplay between T. gondii infection and the mouse hippocampus
2021-01-27 | MTBLS1890 | MetaboLights
Project description:Background. Coagulopathic bleeding is a major cause of mortality after trauma, and platelet dysfunction contributes to this problem. The causes of platelet dysfunction are relatively unknown, but a great deal can be learned from the plasma environment about the possible pathways involved.
Objective. Describe the changes in plasma proteomic profile associated with platelet dysfunction after trauma.
Methods. Citrated blood was collected from severely injured trauma patients at the time of their arrival to the Emergency Department. Samples were collected from 110 patients, and a subset of twenty-four patients was identified by a preserved (n=12) or severely impaired (n=12) platelet aggregation response to five different agonists. Untargeted proteomics was performed by nanoflow liquid chromatography tandem mass spectrometry. Protein abundance levels for each patient were normalized to total protein concentration to control for hemodilution by crystalloid fluid infusion prior to blood draw.
Results. Patients with platelet dysfunction were more severely injured but otherwise demographically similar to those with retained platelet function. Of 232 proteins detected, twelve were significantly different between groups. These proteins fall into several broad categories related to platelet function, including microvascular obstruction with platelet activation, immune activation, and protease activation.
Conclusions. This observational study provides a description of the change in proteomic profile associated with platelet dysfunction after trauma and identifies twelve proteins with the most profound changes. The pathways involving these proteins are salient targets for immediate investigation to better understand platelet dysfunction after trauma and identify targets for intervention.
2021-02-24 | MSV000086948 | MassIVE