MicroRNA expression in R6/2 and wild-type mouse brain
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE100792 | GEO | 2018/04/11
REPOSITORIES: GEO
Similar Datasets
Project description:The expression profiles of miRNAs in klotho-deficient and wild-type mice were examined by means of Genopal®-MICM DNA chips. The data suggested that there was a difference in the expression of miRNAs between klotho-deficient and wild-type mice.
2012-11-01 | GSE34531 | GEO
Project description:The expression profiles of miRNAs in klotho-deficient and wild-type mice were examined by means of GenopalM-BM-.-MICM DNA chips. The data suggested that there was a difference in the expression of miRNAs between klotho-deficient and wild-type mice. Small RNA samples prevared from 5-week-old klotho-deficient and wild-type mice were examined.
2012-11-01 | E-GEOD-34531 | biostudies-arrayexpress
Project description:Using the Cross-linking immuno-precipitation (CLIP) methodology combined with high throughput sequencing analysis, we have identified the RNA targets of the RNA-binding protein RBM5 in the brain of wild-type and R6/2 (Huntington's disease model) adult mice. In parallel, transcriptome analysis was performed by RNA-sequencing using brain samples from the same animals.
2023-06-22 | GSE187445 | GEO
Project description:Huntington’s disease is a genetic disease caused by a single mutation. It is characterised by progressive movement, emotional and cognitive deficits. R6/2 transgenic mice carrying the Huntington’s disease mutation have a progressive neurological phenotype, including deterioration in cognitive function. The mechanism underlying the cognitive deficits in R6/2 mice is unknown, but dysregulated gene expression, reduced neurotransmitter levels and abnormal synaptic function are present before the cognitive decline becomes pronounced. Our goal here was to ameliorate the cognitive phenotype in R6/2 mice using a combination drug therapy (tacrine, moclobemide and creatine) aimed boosting neurotransmitter levels in the brain. Treatment from 5 weeks of age prevented deterioration in two different cognitive tasks until at least 12 weeks. However, motor deterioration continued unabated. Microarray analysis of global gene expression revealed that many genes significantly up- or down-regulated in untreated R6/2 mice had returned towards normal levels after treatment. Thus dysregulated gene expression was reversed by the combination treatment in the R6/2 mice and probably underlies the observed improvements in cognitive function. Our study shows that cognitive decline caused by a genetic mutation can be slowed by a combination drug treatment, and gives hope that cognitive symptoms in HD can be treated. Keywords = HD Keywords = Huntingtin Keywords = cognitive disorder Keywords = R6/2 Keywords = transgenic mice Keywords = gene expression Keywords = microarray Keywords: ordered
2004-06-01 | GSE857 | GEO
Project description:Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntington's disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. We show that HDAC4 reduction delayed cytoplasmic aggregate formation, restored Bdnf transcript levels and rescued neuronal and cortico-striatal synaptic function in HD mouse models. This was accompanied by an improvement in motor co-ordination, neurological phenotypes and increased lifespan. Surprisingly, HDAC4 reduction had no effect on global transcriptional dysfunction and did not modulate nuclear huntingtin aggregation. Our results define a crucial role for cytoplasmic aggregation in the molecular pathology of HD. HDAC4 reduction presents a novel strategy for targeting huntingtin aggregation which may be amenable to small molecule therapeutics. mRNA expression analysis was performed by microarray in 9 weeks old WT (n=9), R6/2 (n=9), HDAC4het (n=9) and Double R6/2::HDAC4het (n=10) mice. Microarray quality control was performed using the software package provided on RACE (http://race.unil.ch).
2014-10-10 | E-GEOD-38218 | biostudies-arrayexpress
Project description:Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntington's disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. We show that HDAC4 reduction delayed cytoplasmic aggregate formation, restored Bdnf transcript levels and rescued neuronal and cortico-striatal synaptic function in HD mouse models. This was accompanied by an improvement in motor co-ordination, neurological phenotypes and increased lifespan. Surprisingly, HDAC4 reduction had no effect on global transcriptional dysfunction and did not modulate nuclear huntingtin aggregation. Our results define a crucial role for cytoplasmic aggregation in the molecular pathology of HD. HDAC4 reduction presents a novel strategy for targeting huntingtin aggregation which may be amenable to small molecule therapeutics. mRNA expression analysis was performed by microarray in 15 weeks old WT (n=8), R6/2 (n=9), HDAC4het (n=8) and Double R6/2::HDAC4het (n=9) mice. Microarray quality control was performed using the software package provided on RACE (http://race.unil.ch).
2014-10-10 | E-GEOD-38219 | biostudies-arrayexpress
Project description:We investigated expression profiles of miRNAs in various tissues of young and elder mice by means of DNA microarray. The results suggested that there was a difference in the expression of miRNAs between young and elder mice.
2012-11-01 | GSE34532 | GEO
Project description:HD R6/1 transgenic mouse line brain hemispheres dissected. RNA targets were created for transgenics and wildtypes at time points 18, 22 and 27 weeks. Profiles and data analysis performed using the Bioconductor software and linear model contrasts using LIMMA on RMA probeset summarys. Keywords: timecourse
2007-07-31 | GSE3621 | GEO
Project description:R6/2 and WT mice treated orally twice a day with vehicle (10% HPβCD), and R6/2 mice treated with either 30 or 100 mg/kg orally twice a day CHDI-00390576. CHDI-00390576 is a Class IIa HDAC inhibitor. Mice were dosed from 4 - 12 weeks of age.
2017-09-23 | GSE104086 | GEO
Project description:We investigated expression profiles of miRNAs in various tissues of young and elder mice by means of DNA microarray. The results suggested that there was a difference in the expression of miRNAs between young and elder mice. Small RNA samples prepareed from various tissues of young and elder mice were examined by means of GenopalM-BM-.-MICM DNA chips.
2012-11-01 | E-GEOD-34532 | biostudies-arrayexpress