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Glucagon contributes to liver zonation in mice

ABSTRACT: Glucagon contributes to liver zonation in mice

PROVIDER: PRJNA434226 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6729560.fastq.gz	Fastqsanger.gz
	SRR6729570.fastq.gz	Fastqsanger.gz
	SRR6729590.fastq.gz	Fastqsanger.gz
	SRR6729561.fastq.gz	Fastqsanger.gz
	SRR6729571.fastq.gz	Fastqsanger.gz

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Glucagon contributes to liver zonation in mice [Gcg infusion]

Project description:Glucagon contributes to liver zonation in mice [Gcg infusion]

| PRJNA434235 | ENA

Glucagon contributes to liver zonation in mice [Gcg KO]

Project description:Glucagon contributes to liver zonation in mice [Gcg KO]

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Glucagon contributes to liver zonation in mice [Gcg infusion]

Project description:Liver zonation characterizes the separation of metabolic pathways along the lobules and is required for optimal function. Wnt/beta-catenin signaling controls metabolic zonation by activating genes in the perivenous hepatocytes, while suppressing genes in the periportal counterparts. We now demonstrate that glucagon opposes the actions of Wnt/beta-catenin signaling on gene expression and metabolic zonation pattern. The effects were more pronounced in the periportal hepatocytes where 28% of all genes were activated by glucagon and inhibited by Wnt/beta-catenin. The glucagon and Wnt/beta-catenin receptors and their signaling pathways are uniformly distributed in periportal and perivenous hepatocytes and the expression is not regulated by the opposing signal. Collectively, our results show that glucagon controls gene expression and metabolic zonation in the liver through a counter play with the Wnt/beta-catenin signaling pathway.

2018-03-01 | GSE110673 | GEO

Glucagon contributes to liver zonation in mice [Gcg KO]

2018-03-01 | GSE110672 | GEO

Glucagon contributes to liver zonation.

Project description:Liver zonation characterizes the separation of metabolic pathways along the lobules and is required for optimal function. Wnt/β-catenin signaling controls metabolic zonation by activating genes in the perivenous hepatocytes, while suppressing genes in the periportal counterparts. We now demonstrate that glucagon opposes the actions of Wnt/β-catenin signaling on gene expression and metabolic zonation pattern. The effects were more pronounced in the periportal hepatocytes where 28% of all genes were activated by glucagon and inhibited by Wnt/β-catenin. The glucagon and Wnt/β-catenin receptors and their signaling pathways are uniformly distributed in periportal and perivenous hepatocytes and the expression is not regulated by the opposing signal. Collectively, our results show that glucagon controls gene expression and metabolic zonation in the liver through a counterplay with the Wnt/β-catenin signaling pathway.

| S-EPMC5924920 | biostudies-literature

Glucagon contributes to liver zonation in mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-03-01 | GSE110674 | GEO

RNAseq liver Glucagon+T3

Project description:21 samples of liver RNA coming from mice treated with glucagon (Gluc), thyroid hormone (T3), both, or the conjugated compound (Cp). Each sample comes from a single mice.

2016-09-28 | GSE85793 | GEO

Glucagon receptor blocked liver gene signature

Project description:Liver RNA-seq in lean or diet-induced obese mice administered with glucagon receptor blocking antibody

2018-11-09 | GSE122348 | GEO

Glucagon receptor deficient liver during postnatal development

Project description:Glucagon receptor deficient liver during postnatal development: fig S5a-S5c in Solloway et al. livers from ko and wt GCGR mice at various developmental stages

2015-06-02 | GSE68141 | GEO

Perturbed liver gene zonation in a mouse model of non-alcoholic steatohepatitis

Project description:Liver zonation characterizes the separation of metabolic pathways along the lobules and is required for optimal hepatic function. Wnt signaling is a master regulator of spatial liver zonation. A perivenous-periportal Wnt activity gradient orchestrates metabolic zonation by activating genes in perivenous hepatocytes, while suppressing genes in their periportal counterparts. The understanding of liver gene zonation and zonation regulators in disease was limited. Non-alcoholic steatohepatitis (NASH) is a chronic liver disease characterized by fat accumulation, inflammation, and fibrosis. Here, we investigated the perturbation of liver gene zonation in a mouse NASH model by combination of spatial transcriptomics, bulk RNAseq and in situ hybridization. Wnt target genes represented a major subset of genes showing altered spatial expression in the NASH liver. The altered Wnt target gene expression level and zonation spatial pattern were in line with the upregulation of Wnt regulators and the augmentation of Wnt signaling. Particularly, we found that the Wnt activator Rspo3 expression was restricted to the perivenous zone in control livers, whereas expanded to the periportal zone in NASH livers. AAV8-mediated RSPO3 overexpression in controls resulted in a zonation change, and further amplified the disturbed zonation of Wnt target genes in NASH, but had no impacts on steatosis, inflammation and fibrosis. In summary, our study demonstrated the alteration of Wnt signaling in a mouse NASH model, leading to perturbed liver zonation.

2024-08-01 | GSE248077 | GEO

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