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Metabolic crosstalk between skeletal muscle cells and liver through IRF4-FSTL1 in nonalcoholic steatohepatitis

ABSTRACT: Metabolic crosstalk between skeletal muscle cells and liver through IRF4-FSTL1 in nonalcoholic steatohepatitis

PROVIDER: PRJNA893368 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22016700.fastq.gz	Fastqsanger.gz
	SRR22016701.fastq.gz	Fastqsanger.gz
	SRR22016702.fastq.gz	Fastqsanger.gz
	SRR22016703.fastq.gz	Fastqsanger.gz
	SRR22016704.fastq.gz	Fastqsanger.gz

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Metabolic crosstalk between skeletal muscle cells and liver through IRF4-FSTL1 in 2 nonalcoholic steatohepatitis

Project description:In this study Guo et al. revealed an endocrine pathway regulated by skeletal muscle IRF4 that manipulates liver pathology. Mice with skeletal muscle specific ablation of IRF4 show ameliorated liver steatosis, inflammation, and fibrosis, without changes in body weight on nonalcoholic steatohepatitis (NASH) diet. Proteomics analysis of mouse serum suggested that follistatin-like protein 1 (FSTL1) might link the communication between muscle and liver. Dual luciferase assays showed that IRF4 could transcriptionally regulate FSTL1 and reconstitution of FSTL1 expression in muscle of F4MKO mice was sufficient to restore the liver pathology. Furthermore, co-culture experiments verified that FSTL1 exerts its function in hepatocyte, macrophage, and hepatic satellite cells through CD14 and DIP2A, CD14, DIP2A, respectively. In human, serum FSTL1 is increased in NASH patients, but the mRNA level of Fstl1 and its receptors are decreased in NASH liver biopsy, suggesting the increased serum FSTL1 is from skeletal muscle as studied in F4MKO mice. These data unveiled a signaling pathway from skeletal muscle to liver via IRF4-FSTL1-DIP2A/CD14 in the pathogenesis of NASH.

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Metabolic crosstalk between skeletal muscle cells and liver through IRF4-FSTL1 in nonalcoholic steatohepatitis

Project description:Inter-organ crosstalk has gained more and more attention recently. However, the mechanisms under this remain incompletely understood. Here, we revealed an endocrine pathway regulated by skeletal muscle IRF4 that manipulates liver pathology. We studied that skeletal muscle specifically deleted IRF4 (F4MKO) mice showed ameliorated liver steatosis, inflammation and fibrosis, without changes in body weight on NASH diet. Proteomics analysis of serum suggested that follistatin-like protein 1 (FSTL1), as a myokine, might linked the communication between skeletal muscle and liver. Dual luciferase assays showed that IRF4 can transcriptionally regulated FSTL1 and reconstitution of FSTL1 expression in skeletal muscle of F4MKO mice, using adeno-associated virus, was sufficient to restore the liver pathology. Furthermore, we performed co-culture experiments to verify different receptors contribute to FSTL1’s function in different cell types of liver. Finally, we found serum FSTL1 level was positively correlated with NASH progression in human, whereas the mRNA level of Fstl1 and its receptors were downregulated in liver biopsy from NASH patients. These data reveal a signaling pathway from skeletal muscle to liver via IRF4-FSTL1-receptors in the pathogenesis of NASH and implicate useful targets for the management of NASH.

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Metabolic crosstalk between skeletal muscle cells and liver through IRF4-FSTL1 in nonalcoholic steatohepatitis.

Project description:Inter-organ crosstalk has gained increasing attention in recent times; however, the underlying mechanisms remain unclear. In this study, we elucidate an endocrine pathway that is regulated by skeletal muscle interferon regulatory factor (IRF) 4, which manipulates liver pathology. Skeletal muscle specific IRF4 knockout (F4MKO) mice exhibited ameliorated hepatic steatosis, inflammation, and fibrosis, without changes in body weight, when put on a nonalcoholic steatohepatitis (NASH) diet. Proteomics analysis results suggested that follistatin-like protein 1 (FSTL1) may constitute a link between muscles and the liver. Dual luciferase assays showed that IRF4 can transcriptionally regulate FSTL1. Further, inducing FSTL1 expression in the muscles of F4MKO mice is sufficient to restore liver pathology. In addition, co-culture experiments confirmed that FSTL1 plays a distinct role in various liver cell types via different receptors. Finally, we observed that the serum FSTL1 level is positively correlated with NASH progression in humans. These data indicate a signaling pathway involving IRF4-FSTL1-DIP2A/CD14, that links skeletal muscle cells to the liver in the pathogenesis of NASH.

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