Endothelial-immune crosstalk contributes to vascular injury in non-alcoholic fatty liver disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA747248 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15175253_1.fastq.gz | Fastqsanger.gz | |||
| SRR15175253_2.fastq.gz | Fastqsanger.gz | |||
| SRR15175254_1.fastq.gz | Fastqsanger.gz | |||
| SRR15175254_2.fastq.gz | Fastqsanger.gz | |||
| SRR15175255_1.fastq.gz | Fastqsanger.gz |
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Project description:Cardiovascular complications are major causes of death in non-alcoholic fatty liver disease (NAFLD) but the underlying endothelial pathophysiology remains understudied. Here, we cultivated blood outgrowth endothelial cells (BOECs) from NAFLD patients and healthy controls. Our transcriptomic analysis revealed that NAFLD BOECs were activated with chemokine hallmarks, in particular, enhanced CXCL12 was confirmed in arterial tissues of mouse NAFLD models. Immunoprofiling by single-cell analysis further uncovered T cell intensification and potentially T-helper type 1 inflammatory reactions in NAFLD. In evaluating CXCL12-CXCR4 axis in chemotaxis, CXCR4 antagonist (AMD3100) substantially modulated the migration of CD4+ T cells, natural killer cells and monocytes towards NAFLD BOECs, which was not observed in healthy control coculture. We found that NAFLD and healthy BOECs might preferentially recruit distinct subsets of immune cells, as a result of unique chemokine ligand-receptor interactions. Finally, we enumerated two folds more circulating endothelial cells, a biomarker of vascular injury, in NAFLD patients than healthy subjects. Our work provides insights for modulation of endothelial-immune crosstalk as an avenue for mitigating endothelial dysfunction in NAFLD.
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Project description:Cardiovascular complications are major causes of death in non-alcoholic fatty liver disease (NAFLD) but the underlying endothelial pathophysiology remains understudied. Here, we cultivated blood outgrowth endothelial cells (BOECs) from NAFLD patients and healthy controls. Our transcriptomic analysis revealed that NAFLD BOECs were activated with chemokine hallmarks, in particular, enhanced CXCL12 was confirmed in arterial tissues of mouse NAFLD models. Immunoprofiling by single-cell analysis further uncovered T cell intensification and potentially T-helper type 1 inflammatory reactions in NAFLD. In evaluating CXCL12-CXCR4 axis in chemotaxis, CXCR4 antagonist (AMD3100) substantially modulated the migration of CD4+ Tcells, natural killer cells and monocytes towards NAFLD BOECs, which was not observed in healthy control coculture. We found that NAFLD and healthy BOECs might preferentially recruit distinct subsets of immune cells, as a result of unique chemokine ligand-receptor interactions. Finally, we enumerated two folds more circulating endothelial cells, a biomarker of vascular injury, in NAFLD patients than healthy subjects. Our work provides insights for modulation of endothelial-immune crosstalk as an avenue for mitigating endothelial dysfunction in NAFLD.
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Project description:Endothelial-immune crosstalk contributes to vasculopathy in nonalcoholic fatty liver disease
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Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes. There are 12 samples in our study which belonged to 4 groups, and each group contains 3 different samples.
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Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes.
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Project description:To elucidate the effect of the polyphenols contained in alcoholic beverages on the metabolic stress induced by ethanol consumption, four groups of mice were fed for five weeks on Lieber's diet with or without ethanol, with ethanol plus ellagic acid, and with ethanol plus trans-resveratrol. Alcoholic fatty liver was observed in the group fed the ethanol diet but not in those fed the ethanol plus polyphenol diets. Liver transcriptome analysis revealed that the addition of the polyphenols suppressed the expression of the genes related to cell stress that were up-regulated by ethanol alone. Conversely, the polyphenols up-regulated the genes involved in bile acid synthesis, unsaturated fatty acid elongation, and tetrahydrofolate synthesis that were down-regulated by ethanol alone. Because parts of these genes were known to be regulated by the constitutive androstane receptor (CAR), we performed the same experiment in the CAR-deficient mice. As a result, fatty liver was observed not only in the ethanol group but also with the ethanol plus polyphenol groups. In addition, there was no segregation of the gene expression profiles among these groups. These results provide a molecular basis for the prevention of alcohol-induced stress by the polyphenols in alcoholic beverages.
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