Genes modulated by DNA demethylation in UM1 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Guo-fu Hu
PROVIDER: E-GEOD-3168 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Primary cortical neurons were isolated from E15 mice and after 5 days in vitro were untreated or treated for 24 h with mesenchymal stem cell conditioned medium and then untreated or treated for a further 24 h with NMDA. Neuron gene expression was profiled and compared between the four different conditions (neurons, neurons+MSC cm, neurons+NMDA, neurons+MSC cm+NMDA) to investigate the molecular mechanisms of MSC neuroprotection. Mesenchymal stem cells (MSC) promote functional recovery in experimental models of central nervous system (CNS) pathology and are currently being tested in clinical trials for stroke, multiple sclerosis and CNS injury. Their beneficial effects are attributed to activation of endogenous CNS repair processes and immune regulation but their mechanisms of action are poorly understood. Here we investigated the neuroprotective effects of MSC in simplified MSC-neuron co-culture systems and in mice using models of glutamate excitotoxicity. MSC protected primary cortical neurons against glutamate (NMDA) receptor-induced death and conditioned medium from MSC (MSC cm), but not control NIH3T3 cells, was sufficient for this effect. MSC cm neuroprotection in mouse cortical neurons was reduced by neutralizing antibodies to bFGF and associated with altered gene expression in neurons towards an immature phenotype as well as reduced neuronal Grin1, Grin2a and Grin2b mRNA levels in response to NMDA stimulation. Further, MSC cm neuroprotection in rat retinal ganglion cells was associated with absence of glutamate-induced calcium influx. Adoptive transfer of EGFP+MSC in a mouse kainic acid seizure model reduced CA3 neuron damage and hippocampal astrocytosis and resulted in the increased expression of neuronal genes that are upregulated by MSC cm, Bmi1, Ddx4, Ezh1, in the hippocampus. These results show that MSC mediate direct neuroprotection against glutamate excitotoxicity by secreting bFGF, reducing glutamate receptor expression and function and altering neuron gene expression towards an immature pattern, and provide evidence for a link between the therapeutic effects of MSC and the activation of endogenous repair processes following CNS injury. In vitro cultures primary cortical neurons from mice were protected from glutamate excitotoxicity when pre-treated with MSC cm. Global gene expression changes induced in neurons before and after treatment with MSC cm and/or NMDA were investigated using a cDNA spotted macroarray filter. Four samples were analysed in duplicate: neurons alone (untreated), neurons+MSC cm, neurons+NMDA, neurons+MSC cm+NMDA.
2011-05-01 | E-GEOD-26279 | biostudies-arrayexpress
Project description:Gene expression profiling in MAPK-related mutants of Magnaporthe oryzae
2012-06-19 | E-MEXP-3658 | biostudies-arrayexpress
Project description:Glycine betaine (GB) is a potent osmoprotectant for salt stressed Bacillus subtilis cells, which possess three high-affinity uptake systems for GB. OpuA is the dominant transporter for this compatible solute. Northern blot analysis, primer extension experiments and opuA-treA reporter gene fusion studies demonstrated that opuA expression is strongly induced at high osmolality from a single SigA-type promoter. Promoter mutations that improve the match of the opuA promoter to the consensus sequence substantially increase basal-level expression but reduce inducibility by high salinity. Expression of opuA is sensitively controlled by GB, which causes significant repression of opuA transcription at low and high salinity. GB influences the kinetics as well as the final level of high salinity induction of opuA in a concentration-dependent fashion. The repressing effect of GB on opuA transcription requires the intracellular presence of GB, regardless whether it is taken up via OpuA or other transporters or synthesized from choline. Genome-wide transcriptional profiling of salt-stressed B. subtilis cells demonstrated that the repressive effect of GB targets only a subset of high-salinity induced genes. This group of GB-responsive genes comprises in essence the full set of genes with demonstrated functions in either the uptake or synthesis of compatible solutes. Four different samples (untreated, GB, NaCl, and GB + NaCl treated) were analyzed and each sample was hybridized in triplicate.
2010-05-15 | E-GEOD-17435 | biostudies-arrayexpress
Project description:We conducted a large-scale gene expression screen using the 3,200 cDNA probe microarray developed specifically for Ursus americanus to detect expression differences in liver and skeletal muscle that occur during winter hibernation in comparison to animals sampled during summer. The expression of 12 genes, including RNA binding protein motif 3 (Rbm3), that are mostly involved in protein biosynthesis, was induced during hibernation in both liver and muscle. The Gene Ontology and Gene Set Enrichment analysis consistently showed a highly significant enrichment of the protein biosynthesis category by over-expressed genes in both liver and skeletal muscle during hibernation. Coordinated induction in transcriptional level of genes involved in protein biosynthesis is a distinctive feature of the transcriptome in hibernating black bears. This finding implies induction of translation and suggests an adaptive mechanism that contributes to a unique ability to reduce muscle atrophy over prolonged periods of immobility during hibernation. Comparing expression profiles in bears to small mammalian hibernators shows a general trend during hibernation of transcriptional changes that include induction of genes involved in lipid metabolism and carbohydrate synthesis as well as depression of genes involved in the urea cycle and detoxification function in liver. Black bears sampled during winter hibernation were compared with the animals sampled during summer. Two tissue types, liver and muscle, were hybridized on a custom 3,200-gene nylon membrane microarray platform with three replicates for each gene (9.600 spots in total). Six hibernating and five summer active bears were studied in experiments with liver tissue, five hibernating and five summer active animals were tested with muscle tissue.
2009-03-09 | E-GEOD-15099 | biostudies-arrayexpress
Project description:We analyzed gene expression in the American black bear, Ursus americanus, using a custom 12,800 cDNA probe (BA02) microarray to detect differences in expression that occur in heart and liver during winter hibernation in comparison to summer active animals. We identified 245 genes in heart and 319 genes in liver that were differentially expressed between winter and summer. The expression of 24 genes was significantly elevated during hibernation in both heart and liver. These genes are mostly involved in lipid catabolism and protein biosynthesis and include RNA binding protein motif 3 (Rbm3), which enhances protein synthesis at mildly hypothermic temperatures. Elevated expression of protein biosynthesis genes suggests induction of translation that may be related to adaptive mechanisms reducing cardiac and muscle atrophies over extended periods of low metabolism and immobility during hibernation in bears. Coordinated reduction of transcription of genes involved in amino acid catabolism suggests redirection of amino acids from catabolic pathways to protein biosynthesis. We identify common for black bears and small mammalian hibernators transcriptional changes in the liver that include induction of genes responsible for fatty acid β oxidation and carbohydrate synthesis and depression of genes involved in lipid biosynthesis, carbohydrate catabolism, cellular respiration and detoxification pathways. Our findings show that modulation of gene expression during winter hibernation represents molecular mechanism of adaptation to extreme environments. Black bears sampled during winter hibernation were compared with the animals sampled during summer. Two tissue types, liver and heart, were hybridized on a custom 12,800 cDNA probe nylon membrane microarray platform . Six hibernating and five summer active bears were studied in experiments with liver tissue, six hibernating and five summer active animals were tested with heart tissue.
2011-05-10 | E-GEOD-27875 | biostudies-arrayexpress
Project description:The study comprises various components: Samples TD: We aims to screen out different gene expression profile in donor biopsies after revascularization , We aims to predict renal allograft dysfunction early after transplantation. Samples AR, ATN, Tx: We aim to screen out different gene expression profile in acute rejection on the kidney. We aim to screen out different gene expression profile in acute tubular necrosis on the kidney. Results from the various study components can help to diagnose renal allograft dysfunction with different causes by distinct gene expression profile. Keywords: acute rejection, acute tubular necrosis, donor biopsies, renal allograft dysfunction Samples AR1-AR17: This study has been accomplished with 17 patients of acute rejection on the kidney.Technical replicates: 2 replicates Samples ATN1-ATN5: This study has been accomplished with 5 patients of acute tubular necrosis on the kidney. Technical replicates: 2 replicates Samples Tx1-Tx14: This study has been accomplished with 14 patients of stable renal function on the kidney.Tecnical replicates:2 replicates(except Tx12) Samples TD1-TD12: This study has been accomplished with 12 patients of donor tissue with stable function early after transplantation on the kidney.Technical replicates: 2 replicates Samples TD13-TD21: This study has been accomplished with 9 patients of donor tissue with renal dysfunction early after transplantation on the kidney.Technical replicates: 2 replicates
2011-02-02 | E-GEOD-26578 | biostudies-arrayexpress
Project description:Role of PPARalpha in the effects of DEHP on the hepatic expression of a selection of mouse genes related to nuclear receptor signaling. Di-(2-ethylhexyl)-phthalate (DEHP), a widely used plasticizer, is detected in consumerâs body fluids. Contamination occurs through environmental and food chain sources. In mouse liver, DEHP activates the peroxisome proliferator-activated receptor alpha (PPARalpha) and regulates the expression of its target genes. Several in vitro investigations support the simultaneous recruitment of additional nuclear receptor pathways. We investigated, in vivo, the hepatic impact of low doses of DEHP on PPARalpha activation, and the putative activation of additional signalling pathways. Wild-type and PPARalpha-deficient mice were exposed to different doses of DEHP. Gene expression profiling delineated the role of PPARalpha and revealed a PPARalpha-independent regulation of several prototypic Constitutive Androstane Receptor (CAR) target genes. This finding demonstrates that CAR also represents a transcriptional regulator sensitive to phthalates. CAR-mediated effects of DEHP provide a new rationale for most endpoints of phthalates toxicity described previously, including endocrine disruption, hepatocarcinogenesis and the metabolic syndrome. Keywords: Treatment effect One-color macroarrays, 6 experimental conditions: Wild type (WT) and PPARalpha-deficient mice (PPAR) were treated with vehicle (Ctrl) or with di-(2-ethylhexyl)-phthalate (DEHP) at 20 mg/kg/day (D20) or 200 mg/kg/day (D200) for 21 days, Biological replicates: 10 for each group, One replicate per array
2010-05-22 | E-GEOD-14920 | biostudies-arrayexpress
Project description:TNF/TNFRI signaling has previously been shown to exert neuroprotective effects after brain ischemic injury. However, the detailed pathways involved remain unidentified. This study aims to identify key neuroprotective molecules activated by TNFRI after permanent ischemic injury in mice. Microarray analysis of the ipsilateral hemispheres of WT and TNFRI knockout at early time points (3 and 6 hours) after the middle cerebral artery occlusion mice were chosen to study the CNS response to injury without significant immune infiltration. Using the ATLAS mouse cDNA arrays that include known genes representative of multiple pathways, we identify novel protective pathways triggered by TNFRI signaling after ischemia. Keywords: brain, ischemic lesion, comparison between WT and TNFRI knockout mice, cDNA array, two different time points (3 and 6 h) RNA was extracted from WT (n=2) and TNFRI KO (n=2) mice at each time point studied (3 and 6 h after ischemia). For each individual sample two hybridisations were performed.
2007-09-04 | E-GEOD-8886 | biostudies-arrayexpress
Project description:Mammalian hibernators display phenotypes similar to physiological conditions in non-hibernating species under conditions of calorie restriction and fasting, hypoxia, hypothermia, ischemia-reperfusion, and sleep. However, whether or how similarities are also reflected on molecular and genetic levels is unclear. We identified molecular signatures of torpor and arousal in hibernation using a new custom-designed cDNA microarray for the arctic ground squirrel (Urocitellus parryii,) and compared them to molecular signatures of selected phenotypes in mouse. Our results show that differential gene expression related to metabolism during torpor is closely related to that during calorie restriction and hypoxia. PPARM-NM-1 is crucial for metabolic remodeling in hibernation. Genes related to the sleep-wake cycle and temperature response genes induced by hypothermia follow the same expression changes as in torpor-arousal cycle. Increased fatty acid metabolism might contribute to the protection against ischemia-reperfusion injury during hibernation. Further, by comparing with thousands of pharmacological signatures, we identified drugs that may induce similar expression patterns in human cell lines as during hibernation. Arctic ground squirrels sampled during winter hibernation were compared with the animals sampled during summer. Liver was hybridized on a custom 9,600 probes nylon membrane microarray platform. Four squirrels in early torpor, five in late torpor, four in early arousal, four in late arousal, and seven in summer active were studied in experiments.
2012-09-01 | E-GEOD-38700 | biostudies-arrayexpress
Project description:Phthalates are industrial additives widely used as plasticizers. In addition to deleterious effects on male genital development, population studies have documented correlations between phthalates exposure and impacts on reproductive tract development and on the metabolic syndrome in male adults. In this study we investigated potential mechanisms underlying the impact of di-(2-ethylhexyl)-phthalate (DEHP) on adult mouse liver in vivo. A parallel analysis of hepatic transcript and metabolic profiles from adult mice exposed to varying DEHP doses was performed. Hepatic genes modulated by DEHP are predominantly PPARα targets. However, the induction of prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways, including Constitutive Androstane Receptor (CAR). Integration of transcriptomic and metabonomic profiles revealed a correlation between the impacts of DEHP on genes and metabolites related to heme synthesis and on the Rev-erbα pathway that senses endogenous heme level. Keywords: Treatment effect One-color macroarrays, 4 experimental conditions: Control mice (vehicle treated), mice treated with di-(2-ethylhexyl)-phthalate (DEHP) at 30 mg/kg/day (D30), 180 mg/kg/day (D180) or 1100 mg/kg/day (D1100) for 14 days, Biological replicates: 6 controls, 4 D30, 4 D180, 5 D1100, One replicate per array
2010-05-05 | E-GEOD-14629 | biostudies-arrayexpress