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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Silencing of microRNAs in mouse liver with "antagomirs

ABSTRACT: Using a novel class of chemically-engineered oligonucleotides, termed "antagomirs", we studied the biological significance of silencing miR-122 in the liver of mice at the mRNA level Experiment Overall Design: Mice were injected on three subsequent days with antagomir-122 or scrambled control (mm-antagomir-122), respectively; 80mg/kg bodyweight/day. 24 hrs after the last treatment, mice were sacrificed and total RNA isolated from the livers. RNA from three mice was pooled and used for generation of biotin-labelled cRNA.

ORGANISM(S): Mus musculus

SUBMITTER: Markus Stoffel

PROVIDER: E-GEOD-3425 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Silencing of microRNAs in vivo with 'antagomirs'.

Krützfeldt Jan J Rajewsky Nikolaus N Braich Ravi R Rajeev Kallanthottathil G KG Tuschl Thomas T Manoharan Muthiah M Stoffel Markus M

Nature 20051030 7068

MicroRNAs (miRNAs) are an abundant class of non-coding RNAs that are believed to be important in many biological processes through regulation of gene expression. The precise molecular function of miRNAs in mammals is largely unknown and a better understanding will require loss-of-function studies in vivo. Here we show that a novel class of chemically engineered oligonucleotides, termed 'antagomirs', are efficient and specific silencers of endogenous miRNAs in mice. Intravenous administration of ...[more]

PMID: 16258535

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Silencing of microRNAs in vivo with "antagomirs"

Project description:Using a novel class of chemically-engineered oligonucleotides, termed "antagomirs", we studied the biological significance of silencing miR-122 in the liver of mice at the mRNA level Keywords: treatment response

2005-11-02 | GSE3425 | GEO

MiR-23b/-27b Targets in Prostate Cancer Cell Lines

Project description:Analysis of genes regulated by miR-23b/-27b overexpression in aggressive PC3-ML cells, confirmed by antagomiR inhibition of miR-23b and miR-27b in the relatively indolent cell line LNCaP. Genes that were downregulated in PC3-ML overexpression and upregulated with LNCaP inhibition were further explored as downstream targets of miR-23b/-27b. PC3-Ml cells were transduced with miR-23b/-27b or a scrambled miRNA control, and only cells expressing greater than 95% transduction efficiency were used for array. LNCaP cells were transfected with antagomiRs to miR-23b and miR-27b, or a non-coding control.

2016-02-10 | E-GEOD-76620 | biostudies-arrayexpress

Gene expression of murine repeatedly activated Th1 cells after miR-31 knock down

Project description:Gene expression of murine repeatedly activated Th1 cells 36h, 48h and 72h after miR-31 inhibition using a specific antagomir (Antagomir-31) compared to a scrambled controll (Antagomir-SCR).

2018-12-19 | GSE122223 | GEO

RNA-seq analysis of livers of C57BL/6 mice upon antagomiR-122 and CL316243 treatment

Project description:Purpose: miR-122 plays a role in lipid metabolism in the liver. The goal of this study is to search for additional metabolic pathways in which miR-122 is involved. Methods: mice were administered with antagomiR-122 (to inhibit miR-122) or antagomiR-control together with CL316243 (β 3-adrenergic receptor agonist, which causes TG hydrolysis to FFAs). Liver mRNAS were generated from 4 mice in each group by deep sequencing using Illumina Nextseq 500 System. The sequence reads that passed quality filters were analyzed with TopHat followed by Cufflinks. The Ingenuity IPA and GeneAnalytics analysis were performed to untangle the biological processes involving the differentially expressed genes. Results: Cufflink algorithm revealed that 182 genes were differentially expressed in the mice livers. According to IPA analysis, the circadian rhythm pathway and adipogenesis were significantly disrupted. Conclutions: Inhibition of miR-122 Activates Several Metabolic Pathways Which Regulate Hepatic Triglycerides Synthesis and Storage

2018-10-10 | GSE87848 | GEO

miR-34a negatively regulates alveolarization in a BPD animal model

Project description:Newborn mice were concomitantly treated with antagomiR-scrambled (SCR) or antagomiR-34a (A34a) and exposed either to normoxia (21% O2) or hyperoxia (85% O2). Lungs were harvested at two different time-points, P5.5 and P14.5, in order to compare the differential mRNA expression between the 4 groups. Unfortunately, few changes in mRNA expression were detected.

2017-02-25 | GSE89730 | GEO

HF liver: Control vs. Plin2-ASO treated

Project description:Transcriptional profiling of mouse liver comparing control, scrambled-oligonucleotides (Cont)-treated mice with Perilipin 2-antisense oligonucleotides (Plin2-ASO)-treated mice. C57BL/6 mice on a high-fat diet were treated with oligonucleotides in vivo. The goal was to determine the effects of Plin2 down-regulation in the liver on global gene expression.

2012-12-05 | GSE37011 | GEO

RNAseq analysis of developing chick somites

Project description:Illumina sequencing was used to characterize the transcriptome of somites dissected from chick embryos HH stage 14-16. Somites were treated as follows: uninjected, injected with antagomiR-206 or with scrambled antagomiR. Transcripts were mapped to the chicken genome.

2019-12-01 | GSE61678 | GEO

Impact of control interventions on lung gene expression in post-natal lung development

Project description:During the studies of post-natal lung development in the laboratory C57BL/6 mouse, broad spectrums of interventions are applied by intraperitoneal (i.p.) injections. We explored whether injection of saline, tamoxifen, “scrambled” antagomiRs (to control studies that target microRNA with antagomiRs), migloyl or water, in well-established protocols, had any impact on the post‑natal gene expression in mouse lungs.

2017-10-02 | GSE92891 | GEO

miRNAs affected by antagomiR-17 treatment

Project description:To understand the the effect of antagomir-17 treatment on human endothelial cells derived from human umbilical cord blood (UCB) CD34+ hematopoietic stem cells, we have employed mRNA sequencing. The antagomiR-17 used in this study was purchased from Dharmacon and cell transfection was performed using Lipofectamine RNAiMAx from Life Technologies. Scramble antagomiR from Ambion was used as control. Cells were transfected with antagomiR-17 or scrambled antagomiR for 48 hours. After 48 h, the cells were collected, RNA was isolated and RNA samples were shipped to Exiqon Services, Denmark for mRNA sequencing. All sequencing experiments (RNA integrity measurements, library preparation and next generation sequencing) were conducted at Exiqon Services, Denmark.

2017-07-07 | GSE76663 | GEO

Assessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance

Project description:Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a miRNA through their binding sites and that changes in ceRNA abundances from individual genes can modulate the miRNA’s activity. Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites. Here, we altered intracellular target-site abundance through expression of a miR-122 target in hepatocytes and livers, and analyzed the effects on miR-122 target genes. Target repression was released in a threshold-like manner at high target-site abundance (≥1.5x10^5 added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA. Furthermore, in response to extreme metabolic liver disease models, global target-site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression. Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect. Seventeen mRNA profiles were generated of 1) primary hepatocytes of mice expressing variable levels of a recombinant Adenovirus expressing the transcript of AldolaseA (Ad-AldoA), containing either 1 or 3 sites matching miR-122 or a mutated miR-122 site (no site), 2) primary hepatocytes derived from mice treated with Antagomir-122 (treatment group) or Antagomir-122mm (control group), 3) livers originating of a genetic model (Ldlr deficient mice) causing severe pathological changes in cholesterol metabolism, 4) livers of mice perfused with Insulin or PBS, and 5) livers of mice fed a high-fat or chow diet; most samples were sequenced in duplicate or triplicate by an Illumina HiSeq 2000. One small RNA profile was also generated from livers of mice fed a chow diet by Solexa sequencing.

2014-05-01 | E-GEOD-52801 | biostudies-arrayexpress

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