Genome-wide analysis of gene expression patterns in mir-122 knockout mice livers
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE27713 | GEO | 2012/08/07
SECONDARY ACCESSION(S): PRJNA138113
REPOSITORIES: GEO
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Project description:To invesigate the physiology roles of mir-122 in liver, we performed expression profiling of mir-122 knockout mice and the control B6/129 mice. Total RNA was extracted from four mir-122 knockout mice and three control mice of 2 months of age. Gene expression was quantified by robust multi-array analysis (RMA) using the Genomic Suite software from Partek.
2012-08-06 | E-GEOD-27713 | biostudies-arrayexpress
Project description:To invesigate the physiological roles of mir-122 in hepatocarcinogenesis, we performed expression profiling of the liver tumors of mir-122 knockout mice and the liver tissues of the control B6/129 mice.
2012-08-07 | GSE31453 | GEO
Project description:To invesigate the physiological roles of mir-122 in hepatocarcinogenesis, we performed expression profiling of the liver tumors of mir-122 knockout mice and the liver tissues of the control B6/129 mice. Total RNA was extracted from three tumors of mir-122 knockout mice and liver tissues of two control mice of 11 months of age; five tumors of mir-122 knockout mice and the liver tissues of three control mice of 14 months of age. Gene expression was quantified by robust multi-array analysis (RMA) using the Genomic Suite software from Partek.
2012-08-06 | E-GEOD-31453 | biostudies-arrayexpress
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
Project description:The liver-specific microRNA, miR-122, is an essential host factor for replication of hepatitis C virus (HCV), an important infectious cause of chronic liver disease and hepatocellular carcinoma. miR-122 stabilizes the positive-strand HCV RNA genome and promotes viral RNA synthesis by binding two closely spaced sites (S1 and S2) near the 5’ end of the genome in association with Ago2. Ago2 is essential for both host factor activities, but whether other host proteins are involved is unknown. Using a quantitative proteomics approach, we identified TNRC6A (GW182) and its paralogs (TNRC6B and TNRC6C), as functionally important components of the miR-122/Ago2 host factor complex binding HCV RNA. Depletion of any two TNRC6 proteins reduced HCV replication in Huh-7.5 cells,but did not reduce viral RNA stability or translational activity, but rather dampened miR-122 stimulation of viral RNA synthesis. However, TNRC6 depletion had no effect on replication of HCV in which S2 was mutated so that miR-122 binds only S1, whereas it significantly enhanced replication when S1 was mutated and only S2 bound by miR-122. Consistent with this, we found that TNRC6 proteins preferentially associate with the S1 site, and that the association of Ago2 with S2 is increased in TNRC6-depleted cells. Collectively, these data suggest a model in which TNRC6 proteins, which are known to interact with Ago2, preferentially direct the miR-122/Ago2 complex to S1 while restricting its association with S2, thereby fine tuning the spatial organization of miR-122/Ago2 complexes bound to the viral RNA.
2019-04-24 | PXD013054 | Pride
Project description:miR-122 is a highly-expressed liver microRNA that is activated perinatally and aids in regulating cholesterol metabolism and promoting terminal differentiation of hepatocytes. Disrupting expression of miR-122 can re-activate embryo-expressed adult-silenced genes, ultimately leading to the development of hepatocellular carcinoma (HCC). We interrogated the liver transcriptome at various time points after genomic excision of miR-122 to determine the cellular consequences leading to oncogenesis. Loss of miR-122 led to specific and progressive increases in expression of imprinted clusters of microRNAs and mRNA transcripts at the Igf2 and Dlk1-Dio3 loci that could be curbed by re-introduction of exogenous miR-122. mRNA targets of other abundant hepatic microRNAs became functionally repressed leading to widespread hepatic transcriptional de-regulation. Together, this reveals a transcriptomic framework for the hepatic response to loss of miR-122 and the outcome on other microRNAs and their cognate gene targets.
2018-10-07 | GSE111805 | GEO
Project description:Liver transcriptome profiling of liver specific miR-122 knockout (miR-122loxP/loxP Alb-Cre) and control (miR-122loxP/loxP) male mice. Expression profile of several hundred mRNAs that include miR-122 targets were altered in miR-122 KO livers. Loss of miR-122 in the germ line resulted in significant changes in hepatic gene expression profile. Among the upregulated genes many are direct targets of miR-122
2012-03-03 | GSE20610 | GEO
Project description:Liver transcriptome profiling of liver specific miR-122 knockout (miR-122loxP/loxP Alb-Cre) and control (miR-122loxP/loxP) male mice. Expression profile of several hundred mRNAs that include miR-122 targets were altered in miR-122 KO livers. Loss of miR-122 in the germ line resulted in significant changes in hepatic gene expression profile. Among the upregulated genes many are direct targets of miR-122 GSM517838-GSM517847: Liver transcriptome profiling of liver specific miR-122 knockout and control male mice. Total liver RNA from 8 week old five control and five liver-specific miR-122 knock out male mice (C57/BL6J background) GSM791601-GSM791604: Liver transcriptome profiling of germ-line miR-122 knockout and control male mice. Liver RNA from 5 week old control (floxed) and miR-122KO mice were analyzed by mouse whole transcriptome profiling.
2012-03-03 | E-GEOD-20610 | biostudies-arrayexpress
Project description:Hepatitis C virus uniquely requires the liver specific microRNA-122 for replication, yet global effects on endogenous miRNA targets during infection are unexplored. Here, high-throughput sequencing and crosslinking immunoprecipitation (HITS-CLIP) experiments of human Argonaute (Ago) during HCV infection showed robust Ago binding on the HCV 5’UTR, at known and predicted miR-122 sites. On the human transcriptome, we observed reduced Ago binding and functional mRNA de-repression of miR-122 targets during virus infection. This miR-122 “sponge” effect could be relieved and redirected to miR-15 targets by swapping the miRNA tropism of the virus. Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and number of sites. We describe a quantitative mathematical model of HCV induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.
2015-01-06 | GSE64679 | 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