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Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis

ABSTRACT: Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis

PROVIDER: PRJNA847972 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19624004_1.fastq.gz	Fastqsanger.gz
	SRR19624004_2.fastq.gz	Fastqsanger.gz
	SRR19624005_1.fastq.gz	Fastqsanger.gz
	SRR19624005_2.fastq.gz	Fastqsanger.gz

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Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis

Project description:Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis

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Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis

Project description:Liver fibrosis results from chronic liver injury triggered by factors such as viral infection, excess alcohol intake, and lipid accumulation. However, the mechanisms underlying liver fibrosis are not fully understood. Here, we demonstrate that expression of Fibroblast growth factor 18 (Fgf18) is elevated in the livers of mice following induction of chronic liver fibrosis models. Deletion and overexpression of Fgf18 in hepatocytes attenuate and promote liver fibrosis, respectively. Single-cell RNA-sequencing revealed that Lrat+ quiescent hepatic stellate cells (HSCs) are increased in the livers of Fgf18 transgenic mice. Mechanistically, FGF18 stimulates the proliferation of quiescent HSCs by inducing the expression of Ccnd1, resulting in the development of liver fibrosis. Moreover, the expression of FGF18 is correlated with the expression of profibrotic genes, such as COL1A1 and ACTA2, in human liver biopsy samples. Thus, FGF18 promotes liver fibrosis and could serve as a therapeutic target to treat liver fibrosis.

2023-09-26 | GSE188273 | GEO

Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis

Project description:Purpose: Analyze the transcriptomic differences between hepatic non parenchimal cells (HNPCs) of Non-Tg and Fgf18 Tg mice Methods: Fresh isolated HNPCs suspensions of Non-Tg and Fgf18 Tg were loaded on the BD RhapsodyTM Single-Cell Analysis System Results: We revealed that CD31-CD34+ cells comprise Lrat+ hepatic stellate cells (HSCs), Acta2+ myofibroblasts, and Thy1+ portal fibroblasts.

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Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis.

Project description:Liver fibrosis results from chronic liver injury triggered by factors such as viral infection, excess alcohol intake, and lipid accumulation. However, the mechanisms underlying liver fibrosis are not fully understood. Here, we demonstrate that the expression of fibroblast growth factor 18 (Fgf18) is elevated in mouse livers following the induction of chronic liver fibrosis models. Deletion of Fgf18 in hepatocytes attenuates liver fibrosis; conversely, overexpression of Fgf18 promotes liver fibrosis. Single-cell RNA sequencing reveals that overexpression of Fgf18 in hepatocytes results in an increase in the number of Lrat+ hepatic stellate cells (HSCs), thereby inducing fibrosis. Mechanistically, FGF18 stimulates the proliferation of HSCs by inducing the expression of Ccnd1. Moreover, the expression of FGF18 is correlated with the expression of profibrotic genes, such as COL1A1 and ACTA2, in human liver biopsy samples. Thus, FGF18 promotes liver fibrosis and could serve as a therapeutic target to treat liver fibrosis.

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