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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE164992 | GEO | 2021/12/31

REPOSITORIES: GEO

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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.

| PRJNA692736 | ENA

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.

2015-03-11 | GSE66745 | GEO

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

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

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.

2012-05-01 | GSE28438 | GEO

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

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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.

2021-12-28 | GSE124473 | GEO

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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Hepatic transcriptome analysis of PRDX1fl/fl and Alb-Cre；PRDX1fl/fl mice on MCD

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2023-08-14 | GSE201030 | GEO

Murine hepatocellular carcinoma of MCL1-/- transgenic mice and age matched alb cre mice - 12 months old.

Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (12 months) and sex matched alb cre mice. Keywords: Array comparative genomic hybridization analysis (aCGH).

2009-12-31 | GSE16580 | GEO

Quantitative proteomic analysis of the livers from 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice.

Project description:We have previously shown that the HyD-LIR-Venus probe can specifically inhibit selective autophagy by suppressing the interaction of LIR-containing selective autophagy substrates and receptors with ATG8-family proteins in vivo. We generated hepatocyte-specific HyD-LIR-Venus-expressing mice (HyD-LIRflox/flox; Alb-Cre) by crossing HyD-LIRflox/flox mice, in which HyD-LIR-Venus is expressed under CAG promoter in a Cre-recombinase-dependent manner, with Alb-Cre transgenic mice that express Cre under the control of the Albumin promoter. We performed quantitative proteomic analysis of the livers of 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice using the RTS-SPS-MS3 method on Tribrid mass spectrometry.

2023-04-24 | PXD037013 | JPOST Repository

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