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Molecular characterization of chronic liver disease dynamics: from liver fibrosis to acute-on-chronic liver failure

ABSTRACT: Molecular characterization of chronic liver disease dynamics: from liver fibrosis to acute-on-chronic liver failure

PROVIDER: PRJNA580468 | ENA |

REPOSITORIES: ENA

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Molecular characterization of chronic liver disease dynamics: from liver fibrosis to acute-on-chronic liver failure

Project description:BACKGROUND: The molecular mechanisms driving the progression from early chronic liver disease (eCLD) to cirrhosis and, finally, acute-on-chronic liver failure (ACLF) are largely unknown. Thus, the aim of this work is to develop a network-based approach to investigate molecular pathways driving progression from eCLD to ACLF. We created 9 liver-specific biological networks capturing key pathophysiological processes potentially related to CLD. We used these networks as framework to perform gene set enrichment analyses(GSEA) and create dynamic profiles of disease progression. RESULTS: Principal component analyses revealed that samples clustered according to the disease stage. GSEA analyses of the defined processes showed an up-regulation of inflammation, fibrosis and apoptosis networks throughout disease progression. Interestingly, we did not find significant gene expression differences between CC and DC, while ACLF showed acute expression changes in all the defined liver-related networks. The analyses of disease progression patterns identified ascending and descending expression profiles associated to ACLF onset. Functional analyses showed that ascending profiles were associated to inflammation, fibrosis, apoptosis, senescence and carcinogenesis networks, while descending profiles were mainly related to oxidative stress and genetic factors. We confirmed by qPCR the up-regulation of 4 genes of the ascending profile CXCL-6, KRT-18, SPINK-1, and ITGA2, and validated our findings on an independent patient’s cohort. CONCLUSION: ACLF is characterized by a specific hepatic gene expression pattern related to inflammation, fibrosis, apoptosis, senescence and carcinogenesis processes. Moreover, the observed profile is significantly different from that of compensated and decompensated cirrhosis, supporting thus the hypothesis that ACLF should be considered a distinct entity.

2021-09-11 | GSE139602 | GEO

Serum EV proteome target analysis of liver fibrosis in chronic hepatitis C patients

Project description:Serum EV proteome target analysis of liver fibrosis in chronic hepatitis C patients was performed.

2023-01-27 | PXD031289 | JPOST Repository

Serum EV proteome non-target analysis of liver fibrosis in chronic hepatitis C patients

Project description:Serum EV proteome non-target analysis of liver fibrosis in chronic hepatitis C patients was performed using TMT-tag quantitation.

2023-01-26 | PXD031283 | JPOST Repository

Liver fibrosis

Project description:Liver fibrosis

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development of prognostic biomarkers for HBV-related acute-on-chronic liver failure

Project description:development of prognostic biomarkers for HBV-related acute-on-chronic liver failure

2020-03-07 | PXD017928 |

Neutrophil Gene expression in Acute-on-chronic liver failure (ACLF), Chronic liver disease (CLD) and Healthy Controls_AIIMSND_Aug2020

Project description:Neutrophil Gene expression in Acute-on-chronic liver failure (ACLF), Chronic liver disease (CLD) and Healthy Controls_AIIMSND_Aug2020

| PRJNA657743 | ENA

Characterization of gene expression profile in HBV-related liver fibrosis patients

Project description:Hepatitis B virus (HBV) infection is a leading risk factor for liver fibrosis (LF) and hepatocellular carcinoma. Emerging evidence indicates that host genetic, virological and immunological factors will influence the fibrotic progress. Many previous studies have focused on specific pathways or genes included in LF mechanism, however global view of the whole genome expresion profile in HBV related LF patients never been studied, and the mechanisms underlying the promotion of liver fibrosis progression remain obscure. Here we collected liver biopsy samples from 124 chronic hepatitis B (CHB) patients and used Affymetrix HG U133 Plus 2.0 microarray to quantify the transcriptome of these patients. Through integrated data analysis, including geneset enrichment analysis (GSEA), weighted gene co-expression analysis (WGCNA), differential expressed gene (DEG) screening, trend test, principle component analysis (PCA) etc., we identified several key pathways and hub genes participated in the initiation and exacerbation of liver fibrotic progress. The function of these hub genes were also validated by in vitro and in vivo experiments using HepG2, Huh7 and LX-2 cell lines and transgenic mice. This is the first large-scale study investigating the gene expression profile in HBV-related LF patients which will be crucial for unlocking the gene functions and gene-gene correlations in fibrosis progress. Liver biopsy samples from 124 CHB patients were collected. The pathological Scheuer Score of each sample were evaluated base on the inflamation and fibrosis severity. Gene expresson of samples in different stage were compared and analyzed. This dataset is part of the TransQST collection.

2016-08-21 | E-GEOD-84044 | biostudies-arrayexpress

Genome-wide DNA methylation dynamics in carbon tetrachloride-induced mice liver fibrosis

Project description:Liver fibrosis was found to be existed in all kinds of chronic liver diseases. Many studies suggested that DNA methylation was related with the pathogenesis of liver fibrosis. The aim of this study was to quantitatively detect DNA methylation changes in the whole genome in fibrotic liver tissues. Carbon tetrachloride (CCl4) was used to induce male mice liver fibrosis by intraperitoneal injection for 4 weeks. A genome-wide methylome analysis was performed using 850K BeadChips assays. The methylation status of 27 CpG dinucleotides located in 3 genes was detected by pyrosequencing to confirm chips data accuracy, and their mRNA expressions were examined by RT-qPCR methods. A total of 130,068 differentially methylated sites (DMS, 58,474 hypermethylated and 71,594 hypomethylated) between fibrotic liver tissues and control mice liver tissues were identified by the 850k BeadChips array. They distribute in each chromosome. Recognition of apoptotic cell, Notch and p38MAPK et al activities were significantly enriched in the Gene Ontology (GO) analyses. Cholesterol metabolism, bile secretion and more biosynthesis and metabolism pathway were enriched in KEGG pathway analyses. Many classical pathways of fibrogenesis and liver activity, as well as more biosynthetic and metabolic pathways, were found to be related to methylation changes. Our result facilitates future research for clinical application.

2023-01-11 | GSE193182 | GEO

Circulating microRNAs associated with liver fibrosis in chronic hepatitis C patients

Project description:Circulating microRNAs associated with liver fibrosis in chronic hepatitis C patients

| PRJNA674765 | ENA

Neutrophil Gene expression in Acute-on-chronic liver failure (ACLF), Chronic liver disease (CLD) and Healthy Controls_AIIMSND_Aug2020

Project description:To address the molecular basis of immune-dysfunction in Acute-on-chronic liver failure (ACLF), we carried out gene expression profiling of blood derived neutrophil from ACLF, belonging to both sterile inflammatory and sepsis conditions. Peripheral whole blood was subjected to PMN enrichment by double gradient centrifugation, and RNA isolation was done by TRIZOL method, followed by microarray experiment using Agilent one-color platform. We compared the gene expression of these neutrophils with that of Chronic liver disease (CLD) patients and healthy controls (HC) for baseline relative quantification, and found unique set of upregulated and downregulated genes in ACLF. We validated the expression of the most differentially expressed genes by quantitative RT-PCR and also stratified the patients into survivors and non-survivors, sepsis and sterile-inflammation. We found an upregulated 3-gene signature of ELANE-MPO-CD177 to be associated with 28-day mortality, irrespective of presence or absence of sepsis.

2021-09-28 | GSE156382 | GEO

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