Serum EV proteome target analysis of liver fibrosis in chronic hepatitis C patients
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens (human)
SUBMITTER: Tetsuo Takehara
PROVIDER: PXD031289 | JPOST Repository | Fri Jan 27 00:00:00 GMT 2023
REPOSITORIES: jPOST
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 200406_HCV_F1_01_200406164121.raw | Raw | |||
| 200406_HCV_F1_02.raw | Raw | |||
| 200406_HCV_F1_03.raw | Raw | |||
| 200406_HCV_F1_04.raw | Raw | |||
| 200406_HCV_F1_05.raw | Raw |
Items per page: 5 1 - 5 of 20 |
Similar Datasets
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
Project description:Circulating microRNAs associated with liver fibrosis in chronic hepatitis C patients
| PRJNA674765 | ENA
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
Project description:Metabolomics offers new insights into disease mechanisms that is enhanced when adopting orthogonal instrumental platforms to expand metabolome coverage, while also reducing false discoveries by independent replication. Herein, we report the first inter-method comparison when using multisegment injection-capillary electrophoresis-mass spectrometry (MSI-CE-MS) and nuclear magnetic resonance (NMR) spectroscopy for characterizing the serum metabolome of patients with liver fibrosis in chronic hepatitis C virus (HCV) infection (<i>n</i> = 20) and non-HCV controls (<i>n</i> = 14). In this study, 60 and 30 serum metabolites were detected frequently (>75%) with good technical precision (median CV < 10%) from serum filtrate samples (<i>n</i> = 34) when using standardized protocols for MSI-CE-MS and NMR, respectively. Also, 20 serum metabolite concentrations were consistently measured by both methods over a 500-fold concentration range with an overall mean bias of 9.5% (<i>n</i> = 660). Multivariate and univariate statistical analyses independently confirmed that serum choline and histidine were consistently elevated (<i>p</i> < 0.05) in HCV patients with late-stage (F2-F4) as compared to early-stage (F0-F1) liver fibrosis. Overall, the ratio of serum choline to uric acid provided optimal differentiation of liver disease severity (<i>AUC</i> = 0.848, <i>p</i> = 0.00766) using a receiver operating characteristic curve, which was positively correlated with liver stiffness measurements by ultrasound imaging (<i>r</i> = 0.606, <i>p</i> = 0.0047). Moreover, serum 5-oxo-proline concentrations were higher in HCV patients as compared to non-HCV controls (<i>F</i> = 4.29, <i>p</i> = 0.0240) after adjustment for covariates (age, sex, BMI), indicative of elevated oxidative stress from glutathione depletion with the onset and progression of liver fibrosis. Both instrumental techniques enable rapid yet reliable quantification of serum metabolites in large-scale metabolomic studies with good overlap for biomarker replication. Advantages of MSI-CE-MS include greater metabolome coverage, lower operating costs, and smaller sample volume requirements, whereas NMR offers a robust platform supported by automated spectral and data processing software.
2023-08-22 | MTBLS3111 | MetaboLights
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 progess.
2016-08-21 | GSE84044 | GEO
Project description:Background & Aims: Chronic HBV patients with concomitant metabolic dysfunction-associated steatohepatitis (MASH) have been shown to develop more advanced fibrosis faster with more severe liver disease as compared to patients with chronic HBV alone. However, our understanding of the underlying mechanisms is limited. Here we study how MASH co-morbidity impact immune activity in the liver of patients with chronic HBV infection. Methods: Bulk RNA sequencing was performed on liver biopsies from patients with only MASH (n=10), only HBeAg-negative chronic HBV (ENEG; n=11), combined MASH/ENEG (n=9) and healthy controls (n=9). Biopsies with no or minimal fibrosis (≤F2) were selected to avoid confounding effects of fibrosis. We compared whole transcriptome data from patients with MASH/ENEG to those with ENEG alone to determine the impact of MASH co-morbidity on chronic hepatitis B. Results: There is a high degree of overlap of liver gene expression profiles in patients with only ENEG versus those with only MASH compared to healthy controls, suggesting a largely shared mechanism of liver dysfunction and immune activity for these distinct conditions. In patients with ENEG, MASH co-morbidity significantly reduced interferon pathway activity (NES=2.03, p.adj=0.0251), the expression of ISGs (e.g., IFIT2, IFI27, IFITM1, IFI6), and macrophage gene signatures (e.g., MARCO, CD163, CD5L, CD63), when compared to patients with ENEG alone. Conclusions: Transcriptomic profiling of the liver suggests that MASH negatively impacts ISGs expression in the liver of patients with ENEG, which may affect antiviral immune pathways, viral replication and inflammatory responses resulting in an increased risk of advanced fibrosis in patients with chronic hepatitis B. Our study provides valuable insights for guiding future research aimed at developing effective, tailored strategies for managing patients with both conditions.
2024-10-31 | GSE274114 | GEO
Project description:In this study, we compared circulating miRNAs identified in hepatitis C virus (HCV)-infected patients presenting two extremes of liver disease: mild/moderate fibrosis and cirrhosis. The patients in the cirrhosis group subsequently developed hepatocellular carcinoma (HCC). Methods: Expression profile of miRNA were identify by semiconductor sequencing using Ion Proton High Power Sequencer. The sequences were exported in FASTQ format for further analysis using the CLC Genomics Workbench software version 8.5. The transcripts were trimmed and then annotated by comparing sequence similarity to miRBASE. After identification of mature miRNAs, differential expression analysis of miRNAs between the mild fibrosis and cirrhosis groups was performed using Empirical Analysis of Differential Gene Expression (EDGE). To verify the potential target genes regulated by the differentially expressed miRNAs identified between the two groups studied, the miRnet tool version 2.0 was applied to identify the regulatory networks in which the miRNAs are involved. Results: We identified 163 mature miRNAs in the mild/moderate fibrosis group and 171 in the cirrhosis group, with 144 in common to both groups. Differential expression analysis revealed 5 upregulated miRNAs and 2 downregulated miRNAs in the cirrhosis group relative to the mild/moderate fibrosis group. Functional analyses of regulatory networks (target gene and miRNA) identified gene categories involved in cell cycle biological processes and metabolic pathways related to cell cycle, cancer, and apoptosis. Conclusion:These results suggest that the differentially expressed circulating miRNAs observed in this work (miR-215-5p, miR-483-5p, miR-193b-3p, miR-34a-5p, miR-885-5p, miR-26b-5p and miR -197-3p) may be candidates for biomarkers in the prognosis of liver disease.
2020-11-06 | GSE160879 | GEO
Project description:As metabolic dysfunction-associated steatotic liver disease (MASLD) frequently co_x0002_occurs in patients with chronic hepatitis B (CHB), the interplay between these two common liver conditions remains largely unexplored. A recent study suggest that MASH comorbidity can reduce intrahepatic interferon pathway activity and macrophage gene signatures in HBeAg_x0002_negative chronic HBV (ENEG) patients, potentially contributing to persistent infection and fibrosis. However, it remains unclear whether this phenomenon also occurs in MASLD with CHB patients.
2025-01-27 | GSE288077 | GEO
Project description:Hepatitis C virus (HCV) infection is an important etiology of chronic liver disease. Multiple possible molecular mechanisms were involved in the progression of liver fibrosis in chronically HCV-infected patients. Therefore, the further revealing novel genes for regulating liver fibrosis might provide evidence for gene diagnosis and molecular-targeted therapy. In this study, we examined the differentially expressed mRNA in plasma samples from the healthy control and patients with HCV-related liver fibrosis, in order to explore the potential predicted and therapeutic target for the development of HCV-related liver fibrosis.
2020-09-10 | GSE154055 | GEO
Project description:Background/Aim: We investigated alterations in the expression of serum exosomal miRNAs with the progression of liver fibrosis and evaluated their clinical applicability as biomarkers. Methods: This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Methods: This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Results: NGS data revealed that exosomal miR-660-5p, miR-125a-5p, and miR-122 expression were changed significantly with the progression of liver fibrosis, of which miR-122 exhibited high read counts enough to be used as a biomarker. The level of exosomal miR-122 decreased as the pathologic fibrosis grade progressed and patients with biopsy-proven advanced fibrosis had significantly lower levels of exosomal miR-122 (P < 0.001) than those without advanced fibrosis. Exosomal miR-122 exhibited a fair performance in discriminating advanced fibrosis especially in combination with fibrosis-4 score and transient elastography. In a subgroup of patients with a non-viral etiology of liver disease, the performance of exosomal miR-122 as a biomarker was greatly improved. Inhibition of miR-122 expression increased the proliferation of the human hepatic stellate cell line, LX-2, and upregulated the expression of various fibrosis related proteins. Conclusion: Exosomal miR-122 may serve as a useful non-invasive biomarker for liver fibrosis, especially in patients with non-viral etiologies of chronic liver disease.
2021-07-15 | GSE179961 | GEO