E-GEOD-52118
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA226719
PROVIDER: E-GEOD-52118 | ExpressionAtlas | 2015-07-27
REPOSITORIES: ExpressionAtlas
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Project description:Comparison of gene expression in motor pools with differential vulnerability in ALS
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Project description:Primary outcome(s): Comparison of the gene expression profile in hair follicle between cancer patients and healthy volunteer
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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. Keywords: disease state analysis
2005-09-23 | GSE3343 | GEO
Project description:Comparison of microarray platforms for measuring differential microRNA expression (Gene Expression data)
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Project description:Numerous genes mutated in amyotrophic lateral sclerosis (ALS) share a role in DNA damage and repair, emphasizing genome disintegration in ALS. DNA instability and repair mechanisms segregate extrachromosomal circular DNAs (ec/eccDNAs) that can modulate gene expression somatically. Here, circulome profiling in a hSOD1G93A genotoxicity model of ALS revealed a 6-fold enrichment of small-size eccDNAs relative to controls. DifCir-based differential analysis identified 189 genes with patterned segregation of differentially produced per gene circles (DPpGCs) from ALS but not from control samples, implicating an inter-sample recurrence rate of at least 89% for the top 6 DPpGCs. Mass spectrometry-based ALS circulome-proteome cross-referencing revealed 31 corresponding differentially expressed proteins (DEPs), with 12 DPpGC-DEP pairs being itemized in ALS risk GWAS databases. DPpGC-DEP hotspots mainly convey neuron-specific functions counteracting ALS detriments. This is unanticipated evidence for non-random, profiled eccDNA accumulation in ALS neurodegeneration, involving putative interactions with their gene products as well as biomarker perspectives.
2023-09-20 | GSE214718 | GEO
Project description:Evaluation of differential gene expression in patients with amyotrophic lateral sclerosis (ALS)
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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:We established iPSCs from healthy donors, FUS-ALS and SOD1-ALS patients. Using our differentiation protocol originally developed by Reinhardt et al.,2013, we diferentiated these iPSCs toward spinal motor neurons (MNs) and reproduce ALS pathology in a dish. To extend our understanding of finding different molecular mechanisms and pathways related to FUS- and SOD mutations in ALS disease, we have performed a comprehensive gene expression profiling study using microarray hybridization of the iPSC-derived MN models from control individuals and carefully compared with those from FUS-ALS and SOD1-ALS patients. In addition, we further analyzed previously published independent datasets containing the genome-wide RNA profiling of iPSC-derived MN samples from patients with FUS and SOD1 mutations and controls. This microaray dataset GSE10638 (Fujimori et al., 2018) was retrieved from GEO database and was screened to identifiy potential drug candidates which suppressed the detected ALS-related phenotypes of these ALS models. Finally, we made a systematic comparison with our results to the ones independently obtained previously.Here through this study, we create a gene profile of ALS by analyzing the differentially expressed genes (DEGs), the kyoto encyclopedia of Genes and Genomes (KEGG) pathways, the interactome as well as transcription factor profiles (TF) that would identify altered functional/molecular signatures and their interactions at both transcriptional (mRNAs) and translational levels (hub proteins and TFs) which stands validation across the different datasets (including different differentiation protocols etc.). By doing so we provide condensed pathophysiological pathways of FUS-ALS and SOD1-ALSto better understand the biological mechanisms underlying motor neuron disease.
2020-09-21 | GSE158264 | GEO