Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA124787 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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: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: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.
2012-08-07 | GSE27713 | 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.
2012-08-07 | GSE31453 | GEO
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:A defining feature of the mammalian liver is polyploidy, a numerical change in the entire complement of chromosomes. The first step of polyploidization involves cell division with failed cytokinesis. Although polyploidy is common, affecting ~90% of hepatocytes in mice and 50% in humans, the specialized role played by polyploid cells in liver homeostasis and disease remains poorly understood. The goal of this study was to identify novel signals that regulate polyploidization, and we focused on microRNAs (miRNAs). First, to test whether miRNAs could regulate hepatic polyploidy we examined livers from Dicer1 liver-specific knockout mice, which are devoid of mature miRNAs. Loss of miRNAs resulted in a 3-fold reduction in binucleate hepatocytes, indicating that miRNAs regulate polyploidization. Secondly, we surveyed age-dependent expression of miRNAs in wild-type mice and identified a subset of miRNAs, including miR-122, that is differentially expressed at 2-3 weeks, a period when extensive polyploidization occurs. Next, we examined Mir122 knockout mice and observed profound, life-long depletion of polyploid hepatocytes, proving that miR-122 is required for complete hepatic polyploidization. Moreover, the polyploidy defect in Mir122 knockout mice was ameliorated by adenovirus-mediated over-expression of miR-122, underscoring the critical role miR-122 plays in polyploidization. Finally, we identified direct targets of miR-122 (Cux1, Rhoa, Iqgap1, Mapre1, Nedd4l and Slc25a34) that regulate cytokinesis. Inhibition of each target induced cytokinesis failure and promoted hepatic binucleation. Conclusion: Our data demonstrate that miR-122 is both necessary and sufficient in liver polyploidization. Among the different signals that have been associated with hepatic polyploidy, miR-122 is the first liver-specific signal identified. These studies will serve as the foundation for future work investigating miR-122 in liver maturation, homeostasis and disease. Livers from C57Bl/6 mice were isolated at defined ages: embryonic day 15.5 (n=3; mixed gender), 2 weeks (n=3; male), 3 weeks (n=3, male) and 7 weeks (n=3; male). Differential miRNA expression was assessed using the nCounter Mouse miRNA Expression Assay Kit (nanoString).
2016-03-29 | E-GEOD-68537 | biostudies-arrayexpress
Project description:Gene expression profiling of HCCs developed in miR-122 knockout mice compared to age-matched wild type mice. The significance of our study is that miR-122 knockout mice spontaneously develop liver tumors and the gene expression profile demonstrated dysregulation of several pathways involved in liver disease and HCC.
2012-08-07 | GSE31731 | GEO
Project description:Gene expression profiling of HCCs developed in miR-122 knockout mice compared to age-matched wild type mice. The significance of our study is that miR-122 knockout mice spontaneously develop liver tumors and the gene expression profile demonstrated dysregulation of several pathways involved in liver disease and HCC. Two-condition experiment, liver tumor vs. normal liver. 8 biological replicates.
2012-08-06 | E-GEOD-31731 | biostudies-arrayexpress
Project description:Adeno-associated viral (AAV) small hairpin (shRNA) expression vectors are a promising therapeutic but can induce severe liver toxicity when delivered at high albeit undefined doses. Using various AAV-shRNA vectors under the high-expressing U6 and low-expressing H1 promoters, we found that dose-limiting toxicity was strongly correlated with an shRNA concentration of >12% of total microRNA levels. Toxicity was associated with a specific reduction in the first synthesized 22nt isoform of miR-122-5p, resulting in the specific de-repression of miR-122 target mRNAs. A causative link between miR-122 reduction and toxicity was established when an AAV-sh-miR-122 vector producing >20% of the total liver miRNAs prevented liver toxicity. Consistent with these results, miR-122 knockout mice, which in part adapt to an absence of miR-122 reduction, also show no toxicity with high dose AAV-shRNA delivery. RNA sequencing of 12 liver samples, 2 receiving H1-shRNAs, 7 with U6-shRNAs and 3 controls; small RNA sequencing of 95 samples including 18 with CMV-driven miR-122 expression in HEK293 cells, 13 in miR-122 knockout mice, 9 samples in mice heterozygous for miR-122, 5 samples with Cre-mediate excision of miR-122, 19 samples immunoprecipitated with Ago2 and 31 additional liver samples (3 control, 11 receiving H1-shRNAs and 17 receiving U6-shRNAs). Small RNA libraries were barcoded (first 4 nucleotides) at the 5' end and ligated to linker-1 (5'-CTGTAGGCACCATCAAT) at the 3' end.
2016-03-09 | E-GEOD-69186 | biostudies-arrayexpress