Stem cell therapy of murine acute hepatitis
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE41465 | GEO | 2012/10/11
SECONDARY ACCESSION(S): PRJNA177111
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression profiles of the liver and hepatic inflammatory cells in murine concanavalin A-induced acute hepatitis models by treatment with adipose tissue derived stem cells C57Bl/6 female mice were treated with adipose tissue-derived stem cells immediately or 3 hours after concanavalin A injection. Two hours later, the liver tissues or hepatic inflammatory cells were obtained and gene expression of them were examined by DNA microarray.
2012-10-11 | E-GEOD-41465 | biostudies-arrayexpress
Project description:Gene expression profiles of the liver and hepatic inflammatory cells in murine non-alcoholic steatohepatitis models by treatment with adipose tissue derived stem cells
2012-08-28 | GSE40395 | GEO
Project description:Gene expression profiles of the liver and hepatic inflammatory cells in murine non-alcoholic steatohepatitis models by treatment with adipose tissue derived stem cells Cirrhotic C57Bl/6 female mice fed by atherogenic high fat diet for 40 weeks were treated with adipose tissue-derived stem cells twice every two weeks. Two weeks later, gene expression of the liver and intrahepatic inflammatory cells were examined by DNA microarray.
2012-08-28 | E-GEOD-40395 | biostudies-arrayexpress
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
2022-03-10 | ST002101 | MetabolomicsWorkbench
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 | ST002098 | MetabolomicsWorkbench
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 | ST002097 | MetabolomicsWorkbench
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
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
2022-03-10 | ST002100 | MetabolomicsWorkbench
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
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.
2015-09-01 | GSE50949 | GEO