Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA139245 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Liver transcriptional profiles of untreated or LPS/GalN-treated wild-type and TMX-/- mice.
2012-05-01 | GSE28438 | GEO
Project description:Liver transcriptional profiles of untreated or LPS/GalN-treated wild-type and TMX-/- mice. 2 genotype, 2 agent sets.
2012-04-30 | E-GEOD-28438 | biostudies-arrayexpress
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.
2024-04-17 | GSE229818 | GEO
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.
2015-03-11 | GSE66745 | GEO
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
Project description:In order to further discover the resistance mechanism of Rack1F/F;Alb-cre mice to LPS/ GalN-induced fulfulant hepatitis, we used genome-wide microarray expression profiling as a discovery platform to identify potential genes associated with resistance to LPS/ GalN-induced in Rack1F/F;Alb-cre mice. Fulminant hepatitis was induced by LPS/GalN in Rack1F/F;Alb-cre mice and Rack1F/F mice for 0, 1,3 and 6 hours, respectively.
2021-12-31 | GSE164992 | GEO
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.
2021-12-28 | GSE124473 | GEO
Project description:D-galactosamine (GalN) and lipopolysaccharide (LPS) effect on GBP5 deficient liver
| PRJNA512115 | ENA
Project description:Gram-negative bacterial infections can cause varying degrees of liver injury in chickens. Although andrographolide has been shown to have a protective effect on the liver, its underlying mechanism of action and effects on liver proteins are not known. The study objectives were to analyze the actions of andrographolide on lipopolysaccharide (LPS)-induced chicken leghorn male hepatoma (LMH) cell injury, identify the different proteins in different groups using TMT proteomics, and explore the pharmacological effects and potential targets of andrographolide in LPS-induced liver injury. It was found that andrographolide reduced alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the cell supernatant and alleviated LPS-induced injury in LMH cells. Proteomic analysis identified 50 and 166 differentially expressed proteins in the LPS vs NC group and LPS-Andro vs LPS group, respectively. Andrographolide may be involved in steroid metabolic processes, negative regulation of MAPK cascade, oxidative stress, and other processes to protect against LPS-induced liver injury. HMGCS1, HMGCR, FDPS, PBK, CAV1, PRDX1, PRDX4, and PRDX6, which were identified by differential proteomics, may be the targets of andrographolide. Our study may provide new theoretical support for andrographolide protection against liver injury.
2022-09-29 | PXD037079 |