Gene profiles during vestibular compensation in unilateral labyrinthectomized rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE32437 | GEO | 2011/11/16
SECONDARY ACCESSION(S): PRJNA147709
REPOSITORIES: GEO
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Project description:Microarray analysis was used to examine the expression of genes upregulated or downregulated in the ipsilateral vestibular nucleus at 1 and 7 days following unilateral labyrinthectomy. Changes in gene expression during the chronic phase of vestibular compensation following unilateral labyrinthectomy in rats Three conditioned experiment: nl:control with sham operation, 1day:1day after labyrninthectomy, 7day:7day after labyrinthectomy
2011-11-16 | E-GEOD-32437 | biostudies-arrayexpress
Project description:To investigate which miRNAs regulate the vestibular compensation after unilateral vestibular deafferentiation (UVD), we have performed microarray for miRNAs as a discovery platform. UVD induces breakdown of the activity of ipsilesional vestibular nuclei and an unbalance of activity between bilateral vestibular nuclei. Vestibular compensation is a course of rebalancing of activities of bilateral vestibular nuclei. It takes place mainly in medial vestibular nucleus. This study was performed using seven week-old-male Sprague–Dawley rats. Based on our previous experiment about vestibular compensation course, we set two time points for harvesting medial vestibular nuclei: 4hr and 4 days after unilateral vestibular deafferentiation. Twenty four animals were divided into two experimental groups: UVD group undergoing UVD at left side (n = 12); and SO group undergoing sham operation (SO) at left side (n=12). Six animals of each group were anesthetized deeply and euthanized at 4 hr or 4 days after surgery, respectively. Medial vestibular nucleus at left side was harvested. Medial vestibular nucleus from three animals became one sample for microarray. Sequentially two samples were obtained for each time point in one group. Microarray for miRNAs was performed using the Agilent Rat miRNA Microarray 8x15K platforms. Considering the fold change of normalized signal intensities between two time points in UVD group and between UVD and SO groups at the same time, miR-31a-5p, 133a-3p, 133b-3p, 204-5p, 206-3p, 218a-5p, 219a-5p, 221-3p and 497-5p were selected as the candidate miRNAs. This result was validated by quantitative reverse transcription-PCR.
2018-02-27 | GSE93111 | GEO
Project description:Gene profiles during vestibular compensation in unilateral labyrinthectomized rats
| PRJNA147709 | ENA
Project description:We performed single-cell RNA-seq of mouse medial vestibular nucleus to reveal the cell diversity of this region.
2023-01-14 | GSE143701 | GEO
Project description:Analysis for unilateral kidney agenesis in heterogenous stock rats
2022-12-05 | PRJEB51993 | EVA
Project description:Vestibular schwannomas are intracranial tumors that affects unilateral and sporadically or bilateral when is associated to Neurofibromatosis type 2 syndrome. The hallmark of the disease is the biallelic inactivation by NF2 gene mutation or LOH of chromosome 22q, where this gene harbors. In this work, we used Infinium HumanMethylation 450K BeadChip microarrays in a series of 36 vestibular schwannomas, 4 non-vestibular schwannomas and 5 healthy nerves. Our results shows a trend to hypomethylation in schwannomas. Furthermore, HOX genes, located at 4 clusters in the genome, displayed hypomethylation in numerous CpG sites in vestibular but not in non-vestibular schwannomas. Additionally, several microRNA and protein-coding genes were found hypomethylated at promoter regions and confirmed by expression analysis; including miRNA-199a1, miRNA-21, MET and PMEPA1. We also detected methylation patterns that might be involved in alternative transcripts of several genes such as NRXN1 or MBP; that would increase the complexity of methylation-expression. Overall, our results shows specific epigenetic signatures in several coding genes and microRNA that could be used in the finding of potential therapeutic targets.
2014-11-30 | GSE56596 | GEO
Project description:Vestibular schwannomas are intracranial tumors that affects unilateral and sporadically or bilateral when is associated to Neurofibromatosis type 2 syndrome. The hallmark of the disease is the biallelic inactivation by NF2 gene mutation or LOH of chromosome 22q, where this gene harbors. In this work, we used Infinium HumanMethylation 450K BeadChip microarrays in a series of 36 vestibular schwannomas, 4 non-vestibular schwannomas and 5 healthy nerves. Our results shows a trend to hypomethylation in schwannomas. Furthermore, HOX genes, located at 4 clusters in the genome, displayed hypomethylation in numerous CpG sites in vestibular but not in non-vestibular schwannomas. Additionally, several microRNA and protein-coding genes were found hypomethylated at promoter regions and confirmed by expression analysis; including miRNA-199a1, miRNA-21, MET and PMEPA1. We also detected methylation patterns that might be involved in alternative transcripts of several genes such as NRXN1 or MBP; that would increase the complexity of methylation-expression. Overall, our results shows specific epigenetic signatures in several coding genes and microRNA that could be used in the finding of potential therapeutic targets.
2014-11-30 | GSE56597 | GEO
Project description:Acute unilateral vestibulopathy (AUV) is the third most common peripheral vestibular disorder after BPPV and Meniere’s disease. Several hypotheses have been proposed for the etiology of AUV including viral infection, vascular occlusion, and autoimmune disease, but the exact pathogenesis still remains unknown. The aim of this study was to investigate the underlying pathogenesis of AUV using the gene expression profiling combined with bioinformatic analysis.
2020-03-03 | GSE146230 | GEO
Project description:Abstract Background Traumatic brain injury (TBI) results in irreversible damage at the site of impact and initiates cellular and molecular processes that lead to secondary neural injury in the surrounding tissue. We used microarray analysis to determine which genes, pathways and networks were significantly altered using a rat model of TBI. Adult rats received a unilateral controlled cortical impact (CCI) and were sacrificed 24h post-injury. The ipsilateral hemi-brain tissue at the site of the injury, the corresponding contralateral hemi-brain tissue, and naïve (control) brain tissue were used for microarray analysis. Ingenuity Pathway Analysis (IPA) software was used to identify molecular pathways and networks that were associated with the altered gene expression in brain tissues following TBI. Results Inspection of the top fifteen biological functions in IPA associated with TBI in the ipsilateral tissues revealed that all had an inflammatory component. IPA analysis also indicated that inflammatory genes were altered on the contralateral side, but many of the genes were inversely expressed compared to the ipsilateral side. The contralateral gene expression pattern suggests a remote anti-inflammatory molecular response. We created a network of the inversely expressed common (i.e., same gene changed on both sides of the brain) inflammatory response (IR) genes and those IR genes included in pathways and networks identified by IPA that changed on only one side. We ranked the genes by the number of direct connections each had in the network, creating a gene interaction hierarchy (GIH). Two well characterized signaling pathways, toll-like receptor/NF-kappaB signaling and JAK/STAT signaling, were prominent in our GIH. Conclusions Bioinformatic analysis of microarray data following TBI identified key molecular pathways and networks associated with neural injury following TBI. The GIH created here provides a starting point for investigating therapeutic targets in a ranked order that is somewhat different than what has been presented previously. In addition to being a vehicle for identifying potential targets for post-TBI therapeutic strategies, our findings can also provide a context for evaluating the potential of therapeutic agents currently in development.
2013-04-12 | GSE45997 | GEO
Project description:Abstract Background Traumatic brain injury (TBI) results in irreversible damage at the site of impact and initiates cellular and molecular processes that lead to secondary neural injury in the surrounding tissue. We used microarray analysis to determine which genes, pathways and networks were significantly altered using a rat model of TBI. Adult rats received a unilateral controlled cortical impact (CCI) and were sacrificed 24h post-injury. The ipsilateral hemi-brain tissue at the site of the injury, the corresponding contralateral hemi-brain tissue, and naM-CM-/ve (control) brain tissue were used for microarray analysis. Ingenuity Pathway Analysis (IPA) software was used to identify molecular pathways and networks that were associated with the altered gene expression in brain tissues following TBI. Results Inspection of the top fifteen biological functions in IPA associated with TBI in the ipsilateral tissues revealed that all had an inflammatory component. IPA analysis also indicated that inflammatory genes were altered on the contralateral side, but many of the genes were inversely expressed compared to the ipsilateral side. The contralateral gene expression pattern suggests a remote anti-inflammatory molecular response. We created a network of the inversely expressed common (i.e., same gene changed on both sides of the brain) inflammatory response (IR) genes and those IR genes included in pathways and networks identified by IPA that changed on only one side. We ranked the genes by the number of direct connections each had in the network, creating a gene interaction hierarchy (GIH). Two well characterized signaling pathways, toll-like receptor/NF-kappaB signaling and JAK/STAT signaling, were prominent in our GIH. Conclusions Bioinformatic analysis of microarray data following TBI identified key molecular pathways and networks associated with neural injury following TBI. The GIH created here provides a starting point for investigating therapeutic targets in a ranked order that is somewhat different than what has been presented previously. In addition to being a vehicle for identifying potential targets for post-TBI therapeutic strategies, our findings can also provide a context for evaluating the potential of therapeutic agents currently in development. The ipsilateral hemi-brain tissue at the site of the injury, the corresponding contralateral hemi-brain tissue, and naM-CM-/ve (control) brain tissue (n=3 for each) were used for RNA isolation. The TBI injured animals were Todd 1, 2 Todd, and Todd 3, each yielding an ispilateral and contralateral sample. The naM-CM-/ve animals were Xu 13 control, Xu 2 control, and Xu 6 control.
2013-04-12 | E-GEOD-45997 | biostudies-arrayexpress