E-MEXP-1406
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-1406 | ExpressionAtlas | 2014-07-03
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MEXP-1406-analysis-methods.tsv | Tabular | |||
| E-MEXP-1406-atlasExperimentSummary.Rdata | Rdata | |||
| E-MEXP-1406-configuration.xml | Xml | |||
| E-MEXP-1406-percentile-ranks.tsv | Tabular | |||
| E-MEXP-1406.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 76 |
Similar Datasets
Project description:Transcription profiling by array of liver from mice fed a high fat diet
2015-10-22 | E-MEXP-1755 | ExpressionAtlas
Project description:The aim of this deep sequencing project is to determine whether treatment of chronically Hepatitis C infected chimpanzees with an antiviral compound leads to accumulation of viral mutants. The liver-expressed microRNA-122 (miR-122) is essential for hepatitis C virus (HCV) RNA accumulation in cultured liver cells, but its potential as a target for antiviral intervention has not been assessed. Here, we show that treatment of chronically infected chimpanzees with a locked nucleic acid (LNA)-modified oligonucleotide (SPC3649) complementary to miR-122 leads to long-lasting suppression of HCV viremia with no evidence for viral resistance or side effects in the treated animals. Furthermore, transcriptome and histological analyses of liver biopsies demonstrated derepression of target mRNAs with miR-122 seed sites, down-regulation of interferon-regulated genes (IRGs) and improvement of HCV-induced liver pathology. The prolonged virological response to SPC3649 treatment without HCV rebound holds promise of a new antiviral therapy with a high barrier to resistance.
2009-12-03 | GSE18919 | GEO
Project description:Antagonism of microRNA-122 in mice by systemically administered LNA-antimiR leads to up-regulation of a large set of predicted target mRNAs in the liver; MicroRNA-122 (miR-122) is an abundant liver-specific miRNA, implicated in fatty acid and cholesterol metabolism as well as hepatitis C viral replication. Here, we report that a systemically administered 16-nt, unconjugated LNA (locked nucleic acid)-antimiR oligonucleotide complementary to the 5' end of miR-122 leads to specific, dose-dependent silencing of miR-122 and shows no hepatotoxicity in mice. Antagonism of miR-122 is due to formation of stable heteroduplexes between the LNA-antimiR and miR-122 as detected by northern analysis. Fluorescence in situ hybridization demonstrated uptake of the LNA-antimiR in mouse liver cells, which was accompanied by markedly reduced hybridization signals for mature miR-122 in treated mice. Functional antagonism of miR-122 was inferred from a low cholesterol phenotype and de-repression within 24 h of 199 liver mRNAs showing significant enrichment for miR-122 seed matches in their 3' UTRs. Expression profiling extended to 3 weeks after the last LNA-antimiR dose revealed that most of the changes in liver gene expression were normalized to saline control levels coinciding with normalized miR-122 and plasma cholesterol levels. Combined, these data suggest that miRNA antagonists comprised of LNA are valuable tools for identifying miRNA targets in vivo and for studying the biological role of miRNAs and miRNA-associated gene-regulatory networks in a physiological context. Experiment Overall Design: Female NMRI mice were treated at day 2 with either 25mg/kg antimiR-122 (SPC3372) or vehicle (saline). Mice were sacrificied at day 3, 9 and 23 and liver RNA assayed. Three biological replicates for each of the six groups.
2009-01-13 | E-GEOD-13948 | biostudies-arrayexpress
Project description:We treated obese mice being fed a high-fat diet with exosomes transfected with a combination of inhibitors of obesity-associated miR-122 and miR-192 and a mimic of exercise-associated miR-133b. We used microarrays to detail the global changes of gene expression induced by the exosomal treatment in liver, adipose and muscle tissues in comparison with HIIT.
2022-11-29 | GSE199465 | GEO
Project description:Antagonism of microRNA-122 in mice by systemically administered LNA-antimiR leads to up-regulation of a large set of predicted target mRNAs in the liver MicroRNA-122 (miR-122) is an abundant liver-specific miRNA, implicated in fatty acid and cholesterol metabolism as well as hepatitis C viral replication. Here, we report that a systemically administered 16-nt, unconjugated LNA (locked nucleic acid)-antimiR oligonucleotide complementary to the 5' end of miR-122 leads to specific, dose-dependent silencing of miR-122 and shows no hepatotoxicity in mice. Antagonism of miR-122 is due to formation of stable heteroduplexes between the LNA-antimiR and miR-122 as detected by northern analysis. Fluorescence in situ hybridization demonstrated uptake of the LNA-antimiR in mouse liver cells, which was accompanied by markedly reduced hybridization signals for mature miR-122 in treated mice. Functional antagonism of miR-122 was inferred from a low cholesterol phenotype and de-repression within 24 h of 199 liver mRNAs showing significant enrichment for miR-122 seed matches in their 3' UTRs. Expression profiling extended to 3 weeks after the last LNA-antimiR dose revealed that most of the changes in liver gene expression were normalized to saline control levels coinciding with normalized miR-122 and plasma cholesterol levels. Combined, these data suggest that miRNA antagonists comprised of LNA are valuable tools for identifying miRNA targets in vivo and for studying the biological role of miRNAs and miRNA-associated gene-regulatory networks in a physiological context. Keywords: compound treatment
2008-12-16 | GSE13948 | GEO
Project description:Liver mRNA microarray study for mice treated with various diets
2015-07-27 | E-GEOD-51885 | ExpressionAtlas
Project description:Expression data from mice on a high fat, high carbohydrate diet treated with exenatide
2015-08-04 | E-GEOD-54774 | ExpressionAtlas
Project description:Transcription profiling by array of liver tissues from mice with liver-specific knockout of Pit1 and wild-type littermates fed with either a high-fat diet or chow control diet
2016-09-23 | E-MTAB-4989 | ExpressionAtlas
Project description:transcription profiling by array of C57BL/6J mice fed a Western-style diet with or without 0.05% quercetin against mice on a control diet to study the effect of quercetin on obesity and hepatic gene expression
2014-10-10 | E-GEOD-38141 | ExpressionAtlas
Project description:To determine the effect of antimiR-122 administration on the mouse miRNome. To functionally investigate a possible link between miR-122 and iron metabolism we inhibited miR-122 by a single, intraperitoneal injection of Locked Nucleic Acid (LNA)-modified antimiR oligonucleotides into age- and sex-matched C57Bl/6 WT mice. To inhibit miR-122 specifically, we injected an antimiR compound with perfect complementarity to miR-122 [perfect match (PM); PM_antimiR-122]. As negative controls, mice were either injected with an LNA control compound with two mismatches (2MM, 2MM_antimiR-122) or the vehicle control (SAL; 0.9% NaCl). Mice were sacrificed three and six weeks after injection. Independent of treatment, mice were viable and exhibited no overt physical or behavioral abnormalities. To exclude that PM_antimiR-122 administration disturbs the expression of other miRNAs we analyzed miRNA expression profiles in the livers, hearts and spleens of the same mice.
2010-10-20 | E-GEOD-24786 | biostudies-arrayexpress