Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Functional metabolomics-based molecular profiling of acute and chronic hepatitis (Serum Metabolomics)

ABSTRACT: Non-alcoholic steatohepatitis (NASH) is a metabolic dysregulation triggered by an overload disrupting the hepatic tolerance to external molecules. With the complexity and diversity of hepatitis triggers, no effective clinical classification and treatment are available, and even using the same strategies or approaches for acute and chronic hepatitis. For us, it is really difficult to precisely diagnose and treat hepatitis accordingly. To overcome this challenge, we integrated metabolomic, lipidomics, transcriptomics and other life science frontier technologies for functional metabolomics studies, and pioneered the redefinition of hepatitis at the molecular level. Our findings suggested that acute hepatitis mainly interferes with purine metabolism and amino acids metabolism, while chronic hepatitis mainly causes disruption of hepatic bile acids and lipidome, especially glycerolipids. Based on the liver-gut axis, we also found that the metabolic regulation of the gut microbiota is another key factor for chronic hepatitis development. In conclusion, functional metabolomics enables the cognition of disease occurrence, development and regression from small molecule metabolic modifications and modulations, realizing the ultimate goal of treating diseases and improving population health through regulation of dysregulated metabolism

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Blood

DISEASE(S): Nash

SUBMITTER: Haitao Lu

PROVIDER: ST002098 | MetabolomicsWorkbench | Wed Mar 09 00:00:00 GMT 2022

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Similar Datasets

Functional metabolomics-based molecular profiling of acute and chronic hepatitis (Stool Metabolomics)

Project description:Non-alcoholic steatohepatitis (NASH) is a metabolic dysregulation triggered by an overload disrupting the hepatic tolerance to external molecules. With the complexity and diversity of hepatitis triggers, no effective clinical classification and treatment are available, and even using the same strategies or approaches for acute and chronic hepatitis. For us, it is really difficult to precisely diagnose and treat hepatitis accordingly. To overcome this challenge, we integrated metabolomic, lipidomics, transcriptomics and other life science frontier technologies for functional metabolomics studies, and pioneered the redefinition of hepatitis at the molecular level. Our findings suggested that acute hepatitis mainly interferes with purine metabolism and amino acids metabolism, while chronic hepatitis mainly causes disruption of hepatic bile acids and lipidome, especially glycerolipids. Based on the liver-gut axis, we also found that the metabolic regulation of the gut microbiota is another key factor for chronic hepatitis development. In conclusion, functional metabolomics enables the cognition of disease occurrence, development and regression from small molecule metabolic modifications and modulations, realizing the ultimate goal of treating diseases and improving population health through regulation of dysregulated metabolism

2022-03-09 | ST002099 | MetabolomicsWorkbench

Functional metabolomics-based molecular profiling of acute and chronic hepatitis (Human Serum Metabolomics)

2022-03-10 | ST002100 | MetabolomicsWorkbench

Functional metabolomics-based molecular profiling of acute and chronic hepatitis (Liver Metabolomics)

2022-03-09 | ST002097 | MetabolomicsWorkbench

Functional metabolomics-based molecular profiling of acute and chronic hepatitis (Liver Lipidomics)

2022-03-10 | ST002101 | MetabolomicsWorkbench

MDSC exacerbate acute hepatitis, mature and loose suppressor function CD40 dependent

Project description:Myeloid-derived suppressor cells (MDSC) represent a heterogeneous population of immature myeloid cells that accumulate in blood, liver, spleen and tumors upon chronic inflammation and tumor development in patients and mice. Acute hepatitis is characterized by a fast infiltration of inflammatory cells in the liver and increased enzymatic activity at this organ that could lead into liver fibrosis and cirrhosis. We have studied the biology of hepatic MDSC in acute hepatitis. Unexpectedly, hepatic MDSC, which accumulate in the liver of mice bearing subcutaneous tumors, failed to suppress inflammatory responses upon Con A injection, but instead were responsible for exacerbating acute liver damage. Phenotypic, genetic and functional studies demonstrated rapid changes of hepatic MDSC from a suppressor phenotype into a pro-inflammatory subset as early as 3 hours after Con A injection. An increase in the expression of pro-inflammatory cytokines, costimulatory molecules such as CD80, CD86 and CD40 along with a loss of suppressor function was noticed in mice upon Con A treatment. These changes were CD40-dependent and not found in CD40-/- MDSC. Interestingly, CD40 ligation of human MDSC in vitro resulted in down-regulation of arginase I expression and suppressor function. Finally, blockade of ROS production in hepatic MDSC ameliorated hepatocyte damage suggesting that MDSC mediated toxicity was ROS dependent. We believe that these findings reflect how MDSC plasticity can be modulated to promote inflammation, opening a new path for therapies targeting innate suppressive cells in cancer patients. EL4 tumors were established in C57BL/6 mice, then mice were injected either with PBS (n=3) or 12.5mg/kg Con A (n=3). Three hours later mice were sacrificed, liver CD11b+Gr-1+ cells were sorted and samples were processed for gene expression analysis.

2015-09-01 | E-GEOD-50949 | biostudies-arrayexpress

MDSC exacerbate acute hepatitis, mature and loose suppressor function CD40 dependent

2015-09-01 | GSE50949 | GEO

Hepatocellular carcinoma follows loss of liver-gender specificity in mice

2007-10-06 | GSE6632 | GEO

Quantitative Proteomic Analysis of Plasma Samples from Chronic Hepatitis B and Chronic Liver Failure Patients for Biomarker Discovery

Project description:Hepatitis B virus (HBV)-associated acute on chronic liver failure (HBV-ACLF), characterized by an acute deterioration of liver function in the patients with chronic hepatitis B (CHB), is lack of predicting biomarkers for prognosis. To explore potential biomarkers of HBV-ACLF for clinical applications, immuno-depletion of high-abundance plasma proteins followed by iTRAQ-based quantitative proteomic approach was employed to analyze plasma samples from 20 healthy control people, 20 CHB patients and 20 HBV-ACLF patients, respectively. As a result, a total of 427 proteins were identified and quantified from these samples, and 42 proteins were differentially expressed in HBV-ACLF patients as compared to both CHB patients and healthy controls. According to bioinformatics analysis results, 6 proteins related to immune response (MMR), inflammatory response (OPN, HPX), blood coagulation (ATIII) and lipid metabolism (APO-CII, GP73) were selected as biomarker candidates. Further ELISA analysis confirmed the significant up-regulation of GP73, MMR, OPN and down-regulation of ATIII, HPX, APO-CII in HBV-ACLF plasma samples (p<0.01). Moreover, receiver operating characteristic (ROC) curve analysis revealed high diagnostic value of these candidates in assessing HBV-ACLF. In conclusion, present quantitative proteomic study identified 6 novel HBV-ACLF biomarker candidates and might provide fundamental information for development of HBV-ACLF biomarker.

2018-10-23 | PXD007975 | Pride

Up-regulated aldo-ketoreductase1B10 in chronic hepatitis C: Association with serum alpha-fetoprotein and hepatocellular carcinoma

Project description:We attempted to identify a specific gene expression signature by performing microarray analysis on the livers of patients with chronic hepatitis C and AFP elevation. Distinct hepatic gene expression patterns were demonstrated between patients with elevated AFP (≥10ng/mL) and normal AFP (<10ng/mL). Among the 30,150 valid genes, 627 were identified as differentially expressed genes with a minimal fold change of 2.0. Using these 627 genes, PCA and HCA were used to successfully distinguish samples according to their AFP status. Of the 627 differently expressed genes, AKR1B10 was most abundantly expressed in patients with elevated AFP. AKR1B10 expression was validated by Real-time RT-PCR and immunohistochemical study. Furthermore, a proportional correlation between AKR1B10 expression and serum AFP was demonstrated by regression analysis. A matched case-control study indicated that AKR1B10 up-regulation was an independent risk factor for HCC development. Liver tissues samples from 48 chronic hepatitis C patients were stratified by their serum AFP levels and analyzed for gene expression profiles. AKR1B10 was up-regulated in patients with chronic hepatitis C in association with serum AFP, and was an independent risk factor for HCC development.

2014-09-15 | E-GEOD-32221 | biostudies-arrayexpress

Transcription profiling of mouse Male A/JCr mice were inoculated with H. hepaticus or vehicle at 4 weeks some underwent castration at 1 year

Project description:We are investigating hepatic transcriptional responses associated with castration and tumorigenic hepatitis induced by Helicobacter hepaticus infection in mature male A/JCr mice; Microarray data demonstrated a global loss of gender-dimorphic gene expression regulation in mice with chronic hepatitis and liver cancer Experiment Overall Design: Male A/JCr mice were inoculated with H. hepaticus or vehicle at 4 weeks; some underwent castration at 1 year, and all were necropsied at 21 months

2008-06-15 | E-GEOD-6632 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data