Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA279383 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cooperative role of Lymphotoxin β Receptor and Tumor Necrosis Factor Receptor p55 in murine liver regeneration (PHx Control vs Enbrel)
| PRJNA300668 | ENA
Project description:Cooperative role of Lymphotoxin Beta Receptor and Tumor Necrosis Factor Receptor p55 in murine liver regeneration
| PRJNA300670 | ENA
Project description:The liver exhibits a unique capacity for regeneration in response to injury. Lymphotoxin β Receptor (LTβR), a core member of the Tumor Necrosis Factor (TNF)/TNF Receptor (TNFR) superfamily is known to play an important role in this process. However, LTβR functions in the pathophysiological alterations and molecular mechanisms of liver regeneration are so far ill-characterized. Interestingly, LTβR / mice suffered from increased and prolonged liver tissue damage after 70 % hepatectomy (PHx), a finding accompanied by elevated alkaline phosphatase levels and deregulated bile acid (BA) homeostasis. Pronounced differences in the expression patterns of genes relevant for BA synthesis and recirculation were observed. Transcriptome analysis revealed a marked disparity in gene expression programs in LTβR / vs. WT liver tissue, where gene ontology (GO) terms related to transcription, gene expression and metabolic pathways were over-represented in the latter. In addition, murinoglobulin 2 (Mug2), a gene product to date not implicated in liver regeneration, was identified as one of the most differentially regulated genes after PHx in WT compared to LTβR / and TNFRp55-/- livers. LTβR and TNFRp55 share downstream signaling elements. TNFRp55 is known to also play an important role in liver regeneration after PHx. Therefore, LTβR / mice were treated with Etanercept to create mice functionally deficient in both signaling pathways. Strikingly, the combined blockade of TNFR and LTβR signaling leads to complete failure of liver regeneration resulting in death within 24 to 48 hours after PHx. LTβR is essential for efficient liver regeneration and cooperates with TNFRp55 in this process. Differences in survival kinetics strongly suggest distinct functions for these two cytokine receptors in liver regeneration. Failure of TNFR and LTβR signaling renders liver regeneration impossible.
2024-02-25 | GSE74531 | GEO
Project description:The liver exhibits a unique capacity for regeneration in response to injury. Lymphotoxin β Receptor (LTβR), a core member of the Tumor Necrosis Factor (TNF)/TNF Receptor (TNFR) superfamily is known to play an important role in this process. However, LTβR functions in the pathophysiological alterations and molecular mechanisms of liver regeneration are so far ill-characterized. Interestingly, LTβR / mice suffered from increased and prolonged liver tissue damage after 70 % hepatectomy (PHx), a finding accompanied by elevated alkaline phosphatase levels and deregulated bile acid (BA) homeostasis. Pronounced differences in the expression patterns of genes relevant for BA synthesis and recirculation were observed. Transcriptome analysis revealed a marked disparity in gene expression programs in LTβR / vs. WT liver tissue, where gene ontology (GO) terms related to transcription, gene expression and metabolic pathways were over-represented in the latter. In addition, murinoglobulin 2 (Mug2), a gene product to date not implicated in liver regeneration, was identified as one of the most differentially regulated genes after PHx in WT compared to LTβR / and TNFRp55-/- livers. LTβR and TNFRp55 share downstream signaling elements. TNFRp55 is known to also play an important role in liver regeneration after PHx. Therefore, LTβR / mice were treated with Etanercept to create mice functionally deficient in both signaling pathways. Strikingly, the combined blockade of TNFR and LTβR signaling leads to complete failure of liver regeneration resulting in death within 24 to 48 hours after PHx. LTβR is essential for efficient liver regeneration and cooperates with TNFRp55 in this process. Differences in survival kinetics strongly suggest distinct functions for these two cytokine receptors in liver regeneration. Failure of TNFR and LTβR signaling renders liver regeneration impossible.
2024-02-25 | GSE67263 | GEO
Project description:p55 and p75 tumor necrosis factor receptor double KO and systemic lupus erythematosis
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Project description:We studied the role of the post-translational modification called O-GlcNAcylation during liver regeneration. Here we generated O-GlcNAc transferase (OGT-KO) and O-GlcNAcase (OGA-KO) hepatocyte-specific knock-out mice. 70% partial hepatectomy (PHX) was performed to induce liver regeneration. We showed that OGA-KO mice had normal liver regeneration whereas OGT-KO mice had a defect in the termination of liver regeneration.
2022-02-25 | GSE188882 | GEO
Project description:Comparison between gene expression profiles of splenic stroma from wild type and lymphotoxin beta receptor knockout mice. The goal was to identify a set of genes which expression in splenic stroma is under lymphotoxin control and which can potentially be important for proper stroma development and function in secondary lymphoid organs. Total RNA isolated from mechanically separated stroma and splenocytes of wild type and LTbR-KO mice, as well as cultured spleen stroma cells from wild type mice. technical replicate - extract: A,B technical replicate - extract: C,D technical replicate - extract: E,F technical replicate - extract: G,H
2013-11-13 | E-GEOD-52294 | biostudies-arrayexpress
Project description:Post-hepatectomy liver failure (PHLF) remains a significant risk for patients undergoing partial hepatectomy (PHx). Reliable prognostic markers and treatments to enhance liver regeneration are lacking. Plasma nanoparticles, including lipoproteins, exosomes, and extracellular vesicles (EVs), can reflect systemic and tissue-wide proteostasis and stress, potentially aiding liver regeneration. Our study included nine patients with hepatocellular carcinoma (HCC) undergoing PHx. Patient plasma was collected before PHx as well as 1 and 5 days after and the EV-protein repertoire was analysed by quantitative mass spectrometry using a super-SILAC mix prepared from primary and cancer cell lines. This longitudinal proteomic analysis of the EVs circulating in the plasma of human patients undergoing PHx uncovers proteomic signatures associated with PHLF, which reflect dying hepatocytes and endothelial cells and were already present before PHx.
2025-08-11 | PXD059885 | Pride
Project description:To identify the Mecp2-dependent transcriptome genome-wide during the very early stage of liver regeneration, we mapped the binding landscape of Mecp2 in control and MeCP2-KO livers before and after PHx using ChIP-seq. we mapped the binding landscape of Mecp2 in control livers before and after PHx by filtering out peaks identified in Mecp2-cKO livers. we identified a total of 14640 and 15350 Mecp2-binding genes before and after PHx in the Mecp2 control liver, respectively.
2024-04-26 | GSE227727 | GEO
Project description:Purpose: We aim to identify changes in the miRNA-ome upon lymphotoxin beta receptor activation Methods: miRNAs were analyzed by sequencing after 2 and 4 days of treatment Results: We could identify different clusters with distinct time-dependent expression after treatment Conclusion: The miRNA-ome is responding on lymphotoxin beta receptor activation
2020-11-30 | GSE161753 | GEO