Transcriptomic signature of spinal cord from SOD1 G86R mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE106364 | GEO | 2018/02/13
REPOSITORIES: GEO
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Project description:mRNA expression in the spinal cords of the G93A-SOD1 familial ALS transgenic mouse model was compared to that in nontransgenic (Normal mouse) and transgenic mice expressing wild-type (WT)SOD1. Gene Ontology (GO)analysis was used to characterize differences in expression between G93A-SOD1 mouse and nontransgenic mouse spinal cord. Changes in multiple GO categories were found. Many of these were associated with subsystems involving cell-cell communication and intracellular signal transduction. Expression profiles of mice expressing WT-SOD1 did not differ from nontransgenic mice. In contrast, protein profiling using proteomics technology indicated changes in mitochondrial protein expression in the G93A-SOD1 mouse spinal cord that were not found in the mRNA expression analysis. Keywords: Disease state analysis, time course, transgenic mice
2006-03-09 | GSE4390 | GEO
Project description:We have investigated the process of disease-induced functional perturbation and the related transcriptional changes occurring in thoraco-lumbar spinal cord extracted from Sprague-Dawley rats heterozygous for the G93A SOD1 gene mutation (Emerging Model 2148 Het Male, Taconic USA; Wyeth and Amyotrophic Lateral Sclerosis Association 2002) using spinal cord from wild type females littermates as reference tissues. Rats were obtained from a breeding project at Taconic Breeding Services (USA). We have applied large-scale gene expression analysis to define the pattern or transcriptional changes occurring in spinal cord from the G93A SOD1 rat model from a pre-symptomatic stage, at disease onset and at end-stage disease, using Bead Array analysis (Illumina, San Diego, USA). We have pooled spinal cord from N:5 transgenic rats for each of the time points considered, using the same pools of spinal cord from sex and age-matched WT rats as reference. In this specific project, the aim was to obtain a gene ontology (GO) pathway analysis of the transcriptional changes induced by the G93A SOD1 mutation in rat spinal cord. Hence, we have opted for a sample pooling strategy, well aware that in so doing, we would not obtaineed information about individuals genes variation across the samples in study but an overall view of the activation of multi-genes molecular signals. Total RNA was isolated from the spinal cords of mutant (G93A SOD1 gene mutation) female rats sacrificed at a pre-symptomatic stage (10-week old), at disease onset and at end stage disease and from age and sex-matched wild type (WT) littermates. RNA samples obtained from spinal cord extracted from rats of the same genetic types and sacrificed at the same time points (e.g. 5 RNA samples from mutant spinal cord from end-stage rats; 5 RNA samples from mutant spinal cord from rats at disease onset; 5 RNA samples from mutant pre-symptomatic rats and 5 RNA samples from spinal cord obtained from age-matched WT rats sacrificed at each of the 3 time points) were pooled and used for gene expression analysis and Ontology analysis of the expression profiles.
2010-06-23 | E-GEOD-20894 | biostudies-arrayexpress
Project description:To investigate the usefulness of gene expression as diagnostic biomarkers, we compared whole genome expression profiles of lumbar spinal cord with profiles of peripheral blood and tibialis anterior muscle in 16 mutant G93A-SOD1 mice and 15 wild type littermates. Total RNA obtained from blood, tibialis anterior muscle and lumbar spinal cord of G93A-SOD1 mice compared to wild type littermates.
2013-03-01 | E-GEOD-27933 | biostudies-arrayexpress
Project description:In this study we investigate how the molecular response to a mechanical stress applied to the spinal cord can be modified by a G93A SOD1 gene mutation, a genetic defect known to cause an invariably fatal form of motor neuron disease. In a 7-day post-injury time period, we perform a 4 time points gene expression profiling of injured spinal cords obtained from pre-symptomatic rats over-expressing the G93A SOD1 gene mutation and from wild type (WT) littermates. The hypothesis tested in this investigation is that the presence of a known genetic defect in a pre-symptomatic rat with a macroscopically normal spinal cord modifies the molecular response to mechanical stress as part of an increase genetically-induced vulnerability to this kind of stress. A better understanding of the molecular mechanisms underlying this susceptibility to trauma may open the way to the uncovering of molecular events which are crucially linked to neurodegenerastion.
2010-06-05 | GSE22161 | GEO
Project description:We have investigated the process of disease-induced functional perturbation and the related transcriptional changes occurring in thoraco-lumbar spinal cord extracted from Sprague-Dawley rats heterozygous for the G93A SOD1 gene mutation (Emerging Model 2148 Het Male, Taconic USA; Wyeth and Amyotrophic Lateral Sclerosis Association 2002) using spinal cord from wild type females littermates as reference tissues. Rats were obtained from a breeding project at Taconic Breeding Services (USA). We have applied large-scale gene expression analysis to define the pattern or transcriptional changes occurring in spinal cord from the G93A SOD1 rat model from a pre-symptomatic stage, at disease onset and at end-stage disease, using Bead Array analysis (Illumina, San Diego, USA). We have pooled spinal cord from N:5 transgenic rats for each of the time points considered, using the same pools of spinal cord from sex and age-matched WT rats as reference. In this specific project, the aim was to obtain a gene ontology (GO) pathway analysis of the transcriptional changes induced by the G93A SOD1 mutation in rat spinal cord. Hence, we have opted for a sample pooling strategy, well aware that in so doing, we would not obtaineed information about individuals genes variation across the samples in study but an overall view of the activation of multi-genes molecular signals.
2010-03-16 | GSE20894 | GEO
Project description:To investigate the usefulness of gene expression as diagnostic biomarkers, we compared whole genome expression profiles of lumbar spinal cord with profiles of peripheral blood and tibialis anterior muscle in 16 mutant G93A-SOD1 mice and 15 wild type littermates.
2013-03-01 | GSE27933 | GEO
Project description:Transcriptomic signature of spinal cord from SOD1 G86R mice
| PRJNA416449 | ENA
Project description:We report transcriptomic dysregulations in the spinal cord of asymptomatic (A: 1.5 months) symptomatic (S: 6 months) and end stage (E: 10-12 months) CHMP2Bintron5 mice by RNA sequencing. We found that genes related to immune system and lipid metabolism had altered expression levels at 1.5 month. Expression of genes related to neuronal system was atletred at 6months and expression of genes related to neuronal system and extracellular matrix xere dfound deregulated at the end-stage. These results were used to determine the change of transcriptomic profile throughout the course of the disease.
2019-12-26 | GSE142590 | GEO
Project description:Amyotrophic lateral sclerosis (ALS) spares the ocular motor system. In this study, we tested the hypothesis that the oculomotor neurons are intrinsically protected in ALS. Using high-density cDNA microarrays, we examined the transcriptome of oculomotor nuclei and spinal cords in mice expressing a human mutant SOD1, the SOD1(G93A) ALS model, at 6 and 10 weeks of age. Comparison of gene expression profiles of these pre-symptomatic SOD1(G93A) mice showed a shift to a proapoptotic state in spinal cords, while the opposite was true in oculomotor nuclei. Seventeen members of the A, B, C and D Hox clusters increased in oculomotor nuclei from 6 to 10 weeks of age; 15 were downregulated in spinal cord. Although only the first 4 classes of a given Hox cluster (e.g., Hoxa1-4) are normally expressed in the developing hindbrain, we found differential expression of mostly the latter classes in both oculomotor nuclei and spinal cords. Also, semaphorin 3B was expressed at 28-fold greater levels in oculomotor nuclei and 61-fold less in spinal cords in 10-week old SOD1(G93A) mice compared to 6-week old mice. Semaphorins 3A and 3E were also differentially regulated. Comparison of gene expression profiles of control SOD1 mice of 6 and 10 weeks of age did not show these changes. Based on these results, we rejected our hypothesis and conclude that the oculomotor nuclei actively adapt to the ALS-inducing mutation.,Supported by NEI and ALSA. <br>Overall design<br>Oligonucleotide microarray studies using the Affymetrix system were conducted as described earlier (McMullen et al., 2004). Biotinylated cRNA was hybridized to Affymetrix Mouse Expression Set 430A GeneChips. Then, the microarrays were washed and stained with a streptavidin-bound marker, and scanned with a laser scanner. Resulting microarray data were analyzed with Affymetrix Microarray Suite 5.0 software. Only those genes with consistent absent/present calls in the three independent replicates per group were considered for further analyses. Comparisons were crossed such that each oculomotor nuclei sample was compared with each spinal cord sample at the corresponding age. The Affymetrix software uses the one-sided Wilcoxons signed rank test to estimate increase/no change/decrease difference calls and fold-changes for each pair-wise comparison. Only difference calls consistent in all pair-wise comparisons and with average changes greater than 2-fold were considered significant, resulting in a conservative list of genes with changed expression levels.
2007-06-28 | E-GEOD-3343 | biostudies-arrayexpress
Project description:In our original grant we proposed to use the NR3B-null mouse model to study the role of NR3B subunit in motor neuron function. We have now successfully generated NR3B null mice. Interestingly, NR3B-null mice invariably die at age P4-P8. Our preliminary examination indicates that the motor strength of these mice is severely impaired prior to death. As we continue to explore the cause of death in NR3B null mice, we propose to conduct gene profiling experiments to search for transcription changes in the brain related to ablation of the NR3B gene. We have used the facility provided by the NINDS/NIMH Microarray Consortium to identify genes that show abnormal expression patterns in these mice. We would like to compare these changes with that opccured in SOD1 mice, a mouse model of motor neuron diseases. Analysis of these genes will help to identify changes in networks and pathways that may cause the death of NR3B-null mice. These studies will further help to elucidate the functional role of NR3B in motor neurons. We will compare samples from motor neurons of wild type and SOD1 mice to identify genes that show abnormal expression patterns, which may be implicated in the death of SOD1 mice and shared with the same changes in NR3B-null mice. We hypothesize that genes with their transcription level changing significantly by ablation of NR3B will be associated with the molecular mechanism underlying the death of motor neurons in NR3B null mice. As NR3B is expressed primarily in the motor neurons of hindbrain and spinal cord, we have first collected and analyzed the spinal cord samples from NR3B null mice and wild-type controls in P4, an age of disease onset. We like to compare motor neuron and spinal cord smaples from SOD1 mice at the age prior to the disease onset. Total RNA from total 12 samples will be purified from ~200 motor neurons obtained by Laser Capture Microdissection and the total spinal cord. Extracted RNAs will be subjected to one or two rounds of amplification and the obtained cRNA will be biotinylated. The purified cRNA will be sent to the NINDS/NIMH Microarray Consortium be used to hybridize the GeneChip Mouse Genome 430 2.0 Array. The hybridization, scanning, and initial data analysis of these GeneChips will be conducted by the Consortium staff. We will analyze the collected data further after data collection. We will first identify genes that show significant changes between wild-type and SOD1 mice and then compare that with the result from NR3B null mice.
2008-06-13 | E-GEOD-5037 | biostudies-arrayexpress