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Endothelial-immune crosstalk contributes to vasculopathy in nonalcoholic fatty liver disease

ABSTRACT: Endothelial-immune crosstalk contributes to vasculopathy in nonalcoholic fatty liver disease

PROVIDER: PRJNA745465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15097803.fastq.gz	Fastqsanger.gz
	SRR15097804.fastq.gz	Fastqsanger.gz
	SRR15097805.fastq.gz	Fastqsanger.gz
	SRR15097806.fastq.gz	Fastqsanger.gz
	SRR15097807.fastq.gz	Fastqsanger.gz

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Endothelial-immune crosstalk contributes to vasculopathy in nonalcoholic fatty liver disease

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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Endothelial-immune crosstalk contributes to vascular injury in non-alcoholic fatty liver disease

Project description:Endothelial-immune crosstalk contributes to vascular injury in non-alcoholic fatty liver disease

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2011-07-07 | E-GEOD-30451 | biostudies-arrayexpress

Endothelial-immune crosstalk contributes to vasculopathy in nonalcoholic fatty liver disease.

Project description:The top cause of mortality in patients with nonalcoholic fatty liver disease (NAFLD) is cardiovascular complications. However, mechanisms of NAFLD-associated vasculopathy remain understudied. Here, we show that blood outgrowth endothelial cells (BOECs) from NAFLD subjects exhibit global transcriptional upregulation of chemokines and human leukocyte antigens. In mouse models of diet-induced NAFLD, we confirm heightened endothelial expressions of CXCL12 in the aortas and the liver vasculatures, and increased retention of infiltrated leukocytes within the vessel walls. To elucidate endothelial-immune crosstalk, we performed immunoprofiling by single-cell analysis, uncovering T cell intensification in NAFLD patients. Functionally, treatment with a CXCL12-neutralizing antibody is effective at moderating the enhanced chemotactic effect of NAFLD BOECs in recruiting CD8+ T lymphocytes. Interference with the CXCL12-CXCR4 axis using a CXCR4 antagonist also averts the impact of immune cell transendothelial migration and restores endothelial barrier integrity. Clinically, we detect threefold more circulating damaged endothelial cells in NAFLD patients than in healthy controls. Our work provides insight into the modulation of interactions with effector immune cells to mitigate endothelial injury in NAFLD.

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