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Myeloid cells in liver and bone marrow acquire a functionally distinct inflammatory phenotype during obesity-related steatohepatitis

ABSTRACT: Myeloid cells in liver and bone marrow acquire a functionally distinct inflammatory phenotype during obesity-related steatohepatitis

PROVIDER: PRJNA545094 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9134390_1.fastq.gz	Fastqsanger.gz
	SRR9134390_2.fastq.gz	Fastqsanger.gz
	SRR9134391_1.fastq.gz	Fastqsanger.gz
	SRR9134391_2.fastq.gz	Fastqsanger.gz
	SRR9134392_1.fastq.gz	Fastqsanger.gz

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Myeloid cells in liver and bone marrow acquire a functionally distinct inflammatory phenotype during obesity-related steatohepatitis

Project description:Myeloid cells in liver and bone marrow acquire a functionally distinct inflammatory phenotype during obesity-related steatohepatitis

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Myeloid cells in liver and bone marrow acquire a functionally distinct inflammatory phenotype during obesity-related steatohepatitis

Project description:Objective: Bone marrow-derived myeloid cells accumulate in the liver as monocytes and macrophages during the progression of obesity-related non-alcoholic fatty liver disease (NAFLD) to steatohepatitis (NASH). Myeloid cells comprise heterogeneous subsets, and dietary overnutrition may affect macrophages in liver and bone marrow. We therefore aimed at characterizing in-depth the functional adaptations of myeloid cells in fatty liver. Design: We employed single-cell RNA-sequencing to comprehensively assess the heterogeneity of myeloid cells in liver and bone marrow during NAFLD, by analyzing C57BL/6 mice fed with a high-fat, high-sugar, high-cholesterol "Western diet" for 16 weeks. We also characterized NAFLD-driven functional adaptations of macrophages in vitro and their functional relevance during steatohepatitis in vivo.

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Myeloid cells in liver and bone marrow acquire a functionally distinct inflammatory phenotype during obesity-related steatohepatitis

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Project description:Core diet-induced obesity networks were constructed using Ingenuity pathway analysis (IPA) based on 332 high-fat diet responsive genes identified in liver by time-course microarray analysis (8 time-points over 24 weeks) of high-fat diet fed mice compared to normal diet fed mice. IPA identified five core diet-induced obesity networks with time-dependent gene expression changes in liver. When we merged core diet-induced obesity networks, Tlr2, Cd14 and Ccnd1 emerged as hub genes associated with both liver steatosis and inflammation and were altered in a time-dependent manner. Further protein-protein interaction network analysis revealed Tlr2, Cd14 and Ccnd1 were inter-related through the ErbB/insulin signaling pathway. Dynamic changes occur in molecular networks underlying diet-induced obesity. Tlr2, Cd14 and Ccnd1 appear to be hub genes integrating molecular interactions associated with the development of NASH. Therapeutics targeting hub genes and core diet-induced obesity networks may help ameliorate diet-induced obesity and NASH. Total RNA obtained from isolated liver of C57BL/6J mice fed normal diet or high fat diet for 0, 2, 4, 6, 8, 12, 16, 20 and 24 weeks.

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Podocytes from Hypertensive and Obese Mice Acquire an Inflammatory, Senescent and Aged Phenotype

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