Transcriptional profiling of PNPase KO liver hepatocytes
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PROVIDER: PRJNA430113 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of PNPase KO liver hepatocytes (HepKO) generated from Albumin-Cre/wt (liver-specific) Pnpt1 fl/fl C57BL/6J mice. Samples comparing liver hepatocyte PNPase KO (HepKO) cells to litter-, age-, and sex-matched wildtype hepatocyte control cells. The goal of this experiment was to determine effects of PNPase loss on the total RNA transcriptome under physiologic in vivo conditions.
2018-05-03 | GSE109210 | GEO
Project description:We generated human liver chimeric mice that were repopulated with human hepatocytes and we infected them for 11 weeks with Hepatitis B virus (HBV). Hepatocytes were isolated from the infected chimeric mouse livers and their gene expressions were compared with those from uninfected chimeric mice using RNA-sequencing.
2020-05-22 | GSE145835 | GEO
Project description:To investigate the role of METTL3-mediated m6A modification in liver, we performed m6A-sequencing and RNA-seq to map the m6A modification and gene expression in liver tissues or hepatocytes of wild type (WT) and liver-sepcific Mettl3-KO mice.
2022-10-29 | GSE207566 | GEO
Project description:Chronic liver inflammation precedes the majority of hepatocellular carcinomas (HCC). Here, we explore the connection between chronic inflammation and DNA methylation in the liver at the late precancerous stages of HCC development in Mdr2/Abcb4-knockout (Mdr2-KO) mice, a model of inflammation-mediated HCC. Using methylated DNA immunoprecipitation (MeDIP) followed by hybridization with Agilent CpG Islands (CGIs) microarrays we found specific CGIs in 76 genes which were hypermethylated in the Mdr2-KO liver compared to age-matched controls. Methylation of thirty among these genes was highly specific to the studied HCC model. We revealed that in most tested cases, the observed hypermethylation resulted from an age-dependent decrease of methylation of the specific CGIs in control livers with no decrease in mutant mice. Chronic inflammation did not change global levels of DNA methylation in Mdr2-KO liver, but caused a 2-fold decrease of the global 5-hydroxymethylcytosine level in mutants compared to controls. This decrease could result from a less efficient age-dependent demethylation of specific CpG sites in the liver of Mdr2-KO mutants, as described above. Expression of some tested hypermethylated genes was increased in Mdr2-KO livers compared to controls (28%), others were either similarly expressed (44%), or not expressed in the liver (28%). Liver cell fractionation revealed, that the relative hypermethylation of specific CGIs in Mdr2-KO compared to control livers affected either hepatocyte, or non-hepatocyte, or both fractions. There was only episodic correlation between changes of gene methylation and expression in cell fractions. Conclusion: Chronic liver inflammation causes hypermethylation of specific CGIs, which may affect both hepatocytes and non-hepatocyte liver cells. These changes may serve as markers of an increased regenerative activity and of a precancerous microenvironment in the chronically inflamed liver. Two-condition experiment, Mdr2-KO vs Mdr2-/+ liver tissue from 12m-old male FVB strain mice. Biological replicates: 3 control replicates, 3 knockout replicates.
2015-03-01 | E-GEOD-64097 | biostudies-arrayexpress
Project description:Liver regeneration is an well orchestrated compensatory process that regulated by multiple factors. We recently reported the importance of chromatin protein, a high-mobility group box 2 (HMGB2) in mouse liver regeneration, however, it’s molecular mechanism is not yet understood. In this study, we aimed to study how HMGB2 regulates hepatocyte proliferation during liver regeneration. Wild-type (WT) and HMGB2-knockout (KO) mice were 70% partial hepatectomized (PHx), and liver tissues were analyzed by microarray, immunohistochemistry, qPCR and western blotting. In vivo experimental findings were confirmed by in vitro experiments using HMGB2 gene knockdown in combination with de novo lipogenesis model. In WT mouse, HMGB2-positive hepatocytes were co-localized with cell proliferation markers, whereas, hepatocyte proliferation was significantly decreased in HMGB2-KO mice. Oil red-O staining detected the transient accumulation of lipid droplets at 12-24 h in WT mouse livers, however, decreased amount of lipid droplets were found in HMGB2-KO mouse livers, and it was prolonged until 36 h. Microarray, immunohistochemistry and qPCR results were demonstrated that lipid metabolism related genes were significantly decreased in HMGB2-KO mouse livers. In vitro experiments demonstrated that decreased lipid droplets in HMGB2-knockdown cells correlated with decreased cell proliferation activity. HMGB2 is involved in the regulation of liver regeneration through transient accumulation of lipid droplets in hepatocytes.
2023-10-14 | GSE244551 | GEO
Project description:In the project « VLK in liver protection », we analyzed conditioned medium and whole cell lysate of Y/A/C-treated hepatocytes isolated from wildtype (WT) and VLK knockout (KO) mice, three biological replicates each.
2022-03-24 | PXD031378 | Pride
Project description:Thiele2013 - Liver hepatocytes
The model of liver hepatocytes metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
Recon 2 we predicted changes in metabolite biomarkers for 49 inborn errors of metabolism with 77% accuracy when compared to experimental data. Mapping metabolomic
data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110014
.
To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
2005-01-01 | MODEL1310110014 | BioModels
Project description:Chronic liver inflammation precedes the majority of hepatocellular carcinomas (HCC). Here, we explore the connection between chronic inflammation and DNA methylation in the liver at the late precancerous stages of HCC development in Mdr2/Abcb4-knockout (Mdr2-KO) mice, a model of inflammation-mediated HCC. Using methylated DNA immunoprecipitation (MeDIP) followed by hybridization with Agilent CpG Islands (CGIs) microarrays we found specific CGIs in 76 genes which were hypermethylated in the Mdr2-KO liver compared to age-matched controls. Methylation of thirty among these genes was highly specific to the studied HCC model. We revealed that in most tested cases, the observed hypermethylation resulted from an age-dependent decrease of methylation of the specific CGIs in control livers with no decrease in mutant mice. Chronic inflammation did not change global levels of DNA methylation in Mdr2-KO liver, but caused a 2-fold decrease of the global 5-hydroxymethylcytosine level in mutants compared to controls. This decrease could result from a less efficient age-dependent demethylation of specific CpG sites in the liver of Mdr2-KO mutants, as described above. Expression of some tested hypermethylated genes was increased in Mdr2-KO livers compared to controls (28%), others were either similarly expressed (44%), or not expressed in the liver (28%). Liver cell fractionation revealed, that the relative hypermethylation of specific CGIs in Mdr2-KO compared to control livers affected either hepatocyte, or non-hepatocyte, or both fractions. There was only episodic correlation between changes of gene methylation and expression in cell fractions. Conclusion: Chronic liver inflammation causes hypermethylation of specific CGIs, which may affect both hepatocytes and non-hepatocyte liver cells. These changes may serve as markers of an increased regenerative activity and of a precancerous microenvironment in the chronically inflamed liver.
2015-03-01 | GSE64097 | GEO
Project description:Polynucleotide phosphorylase (PNPase) is an essential mitochondria-localized exoribonuclease implicated in multiple biological processes and several human disorders. To reveal role(s) for PNPase in mitochondria, we established PNPase knockout (PKO) systems by first shifting culture conditions to enable cell growth with defective respiration. PKO resulted in loss of mitochondrial DNA (mtDNA) and a transcriptional profile similar to rho0 mtDNA deleted cells, with perturbations in cholesterol, lipid, and secondary alcohol metabolic pathways. PKO cells also showed growth and cell cycle profiles similar to rho0 cells. PKO in mouse inner ear hair cells cause progressive hearing loss that parallel human familial hearing loss previously linked to mutations in PNPase. Combined, our data suggest that mtDNA maintenance could provide a unifying connection for the large number of biological activities reported for PNPase.
2018-05-01 | GSE111668 | GEO
Project description:PNPase is the primary RNA turnover enzyme in Bacillus subtilis and plays a crucial role in regulating gene expression. To investigate the life activities that PNPase participated in Bacillus subtilis 9407, RNA immunoprecipitation-sequencing (RIP-seq) analysis was performed to pinpoint the direct RNA targets of PNPase using 6×his-tagged PNPase (PNPase group) and PNPaseD493A (D493A group) constructs that were driven by the IPTG-induced Pgrac promoter.
2023-09-20 | GSE243342 | GEO