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Expression analysis of liver tissues from LPS or LPS/GalN treated mice

ABSTRACT: Investigation of whole genome gene expression level changes in the liver tissue from LPS/GalN treated mice, compared to LPS treated mice Treatment of mice with LPS and the liver-specific transcriptional inhibitor D-(+)-galactosamine (GalN) induces fatal hepatitis, which is mediated by TNFα and characterized by massive hepatic apoptosis. Previous studies suggest that GalN increases the sensitivity to LPS/TNFα probably by blocking the transcription of protective factors, but the identity of most of these factors is still unclear. This analysis is performed to indentify these protective factors.

ORGANISM(S): Mus musculus

PROVIDER: GSE66745 | GEO | 2015/03/11

SECONDARY ACCESSION(S): PRJNA277851

REPOSITORIES: GEO

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Expression analysis of liver tissues from LPS or LPS/GalN treated mice

Project description:Investigation of whole genome gene expression level changes in the liver tissue from LPS/GalN treated mice, compared to LPS treated mice Treatment of mice with LPS and the liver-specific transcriptional inhibitor D-(+)-galactosamine (GalN) induces fatal hepatitis, which is mediated by TNFα and characterized by massive hepatic apoptosis. Previous studies suggest that GalN increases the sensitivity to LPS/TNFα probably by blocking the transcription of protective factors, but the identity of most of these factors is still unclear. This analysis is performed to indentify these protective factors. A six chip study using total RNA extracted from liver tissues of three separate LPS treated mice and three separate LPS/GalN treated mice. Each chip measures the expression level of 44,170 genes from C57 BL/6 mice with three 60-mer probe pairs per gene.

2015-03-11 | E-GEOD-66745 | biostudies-arrayexpress

Comparision of LPS/GalN-induced gene expression in Rack1F/F and Rack1F/F;Alb-cre livers.

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D-galactosamine (GalN) and lipopolysaccharide (LPS) effect on GBP5 deficient liver

Project description:D-galactosamine (GalN) and lipopolysaccharide (LPS) effect on GBP5 deficient liver

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LPS/GalN-induced liver injury model: wild-type vs. TMX-deficient mice

Project description:Liver transcriptional profiles of untreated or LPS/GalN-treated wild-type and TMX-/- mice. 2 genotype, 2 agent sets.

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D-galactosamine (GalN) and lipopolysaccharide (LPS) effect on GBP5 deficient liver

Project description:Purpose: The goal of this study is to compare transcriptome profilings of liver from GBP5 knockout and WT control mice treated with GalN/LPS. Methods: GBP5 knockout and WT control mice were treated with GalN (800 μg/g body weight) and LPS (100 ng/g body weight) for 6 h to induce liver inflammation and injury. RNA samples were pooled from livers of GBP5 KO and WT mice (n=4 for each group). RNA-seq was performed by using HiSeq X Ten platform. Paired-end clean reads were aligned to the mouse reference genome (Ensembl_GRCm38.89) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of liver transcriptomes from GBP5 KO and WT mice treated with GalN/LPS, generated by RNA-seq technology. The RNA-seq analysis showed that 405 genes were down-regulated and 33 genes were up-regulated in the liver of GBP5 KO mice. GO analysis showed that the down-regulated genes were primarily related to the immune system process and response to stress. KEGG pathway enrichment analysis showed that phagocytosis and Jak-STAT signaling pathway were significantly decreased in the liver of GBP5 KO mice.

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Meyoid-specific deficiency of Glutamine Synthetase Aggravates LPS/D-GalN-induced liver injury via the activation of monocyte-derived macrophages

Project description:Glutamine synthase (Glul) is a key enzyme to synthesize glutamine, but its function in acute liver injury (ALI) remains unclear. Here, we investigated the regulatory role of Glul on immnuity in LPS/D-GalN-induced ALI. The study firstly found that the expression of Glul in myeloid cells was inhibited following LPS/D-GalN challenge. Then myeloid-specific knockout Glul mice were generated, which showed more severe ALI and higher mortality due to the activation of monocyte-derived macrophages (MoMFs) and the secretion of CCL2, as well as the recruitment of CCR2+ monocytes. Notably, liver injury can be relieved with adeno-associated virus (AAV)-mediated hepatic delivery of Glul via tail vein injection in mice. In conclusion, this research validates the protective effect of Glul against ALI.

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Transcriptomic profiling of differentially expressed mRNA in liver tissue of Dgaln/LPS induced liver injury mice [mRNA_Dgaln]

Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide(Dgaln/lps), APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates Dgaln/lps-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against Dgaln/lps-induced hepatocyte injury.

2023-09-01 | GSE241513 | GEO

Comparision of LPS/GalN-induced gene expression in Rack1F/F and Rack1F/F Alb-cre livers.

Project description:Comparision of LPS/GalN-induced gene expression in Rack1F/F and Rack1F/F Alb-cre livers.

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Comparative proteomic analyses of the liver in D-galactosamine sensitized mice treated with different toll-like receptor agonists

Project description:Acute liver failure (ALF) is a severe consequence of abrupt hepatocyte injury with lethal outcomes. Three toll-like receptor (TLR) agonists, including polyinosinic-polycytidylic acid [poly(I:C)], lipopolysaccharide (LPS), and cytosine-phosphate-guanine oligonucleotide (CpG ODN), respectively, cause severe and acute hepatitis in D-galactosamine (D-GalN) sensitized mice as the experimental ALF animal models. However, the molecular differences in ALF among the three models are unclear. Here, we conducted global proteomic analyses of the three ALF mice models. We identified 227, 321, and 114 differentially regulated proteins and 80,195, and 23 specifically expressed proteins in the poly(I:C)/D-GalN, LPS/D-GalN and CpG ODN/D-GalN groups compared to the control group, respectively. Fifty-two proteins were commonly identified in the three ALF groups. Gene ontology (GO) analyses showed that 45 proteins were located in organelles, 35 proteins were involved in metabolic processes, and 10 proteins were involved in immune system processes. Poly (I:C)- and LPS-specific proteins were mainly distributed in the membrane and endoplasmic reticulum, respectively. LPS-specific proteins were more enriched in metabolic pathways. CpG-specific proteins were mainly related to the ribosome structural composition. In conclusion, our study shows different molecular mechanisms of three TLR agonists in D-GalN induced ALF and provides a useful dataset for the guidance of future studies.

2020-01-19 | PXD017180 |

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