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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: PRJNA534228 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8944480.fastq.gz	Fastqsanger.gz
	SRR8944490.fastq.gz	Fastqsanger.gz
	SRR8944471.fastq.gz	Fastqsanger.gz
	SRR8944481.fastq.gz	Fastqsanger.gz
	SRR8944491.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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Project description:Patients with hypertension or obesity can develop glomerular dysfunction characterized by injury and depletion of podocytes. To better understand the molecular processes involved, young mice were treated with either deoxycorticosterone acetate (DOCA) or fed a high-fat diet (HFD) to induce hypertension or obesity, respectively. The transcriptional changes associated with these phenotypes were measured by unbiased bulk mRNA-sequencing of isolated podocytes from experimental models and their respective controls. Key findings were validated by immunostaining. In addition to a decrease in canonical proteins and reduced podocyte number, podocytes from both hypertensive and obese mice exhibited a sterile inflammatory phenotype characterized by increases in NLRP3 inflammasome, protein cell death-1, and Toll-Like Receptor pathways. Finally, although the mice were young, podocytes in both models exhibited increased expression of senescence and aging genes, including genes consistent with a senescence-associated secretory phenotype. However, there were differences between the hypertension- and obesity-associated senescence phenotypes. Both show stress-induced podocyte senescence characterized by increased p21 and p53. Moreover, in hypertensive mice, this is superimposed upon age-associated podocyte senescence characterized by increased p16 and p19. These results suggest that senescence, aging, and inflammation are critical aspects of the podocyte phenotype in experimental hypertension and obesity in mice.

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