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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

| PRJNA778176 | ENA

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.

2023-09-20 | GSE205871 | GEO

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.

| S-EPMC10562492 | biostudies-literature

miR-182-5p Promotes Hepatocyte-Stellate Cell Crosstalk to Facilitate Liver Regeneration

Project description:A unique feature of the liver is its high regenerative capacity, which is essential to maintain liver homeostasis. However, key regulators of liver regeneration (LR) remain ill-defined. Here, we identify hepatic miR-182-5p as a key regulator of LR. Suppressing miR-182-5p, whose expression is significantly induced in the liver of mice post two-thirds partial hepatectomy (PH), abrogates PH-induced LR in mice. In contrast, liver-specific overexpression of miR-182-5p promotes LR in mice with PH. Overexpression of miR-182-5p failed to promote proliferation in hepatocytes, but stimulates proliferation when hepatocytes are cocultured with stellate cells. Mechanistically, miR-182-5p stimulates Cyp7a1-mediated cholic acid production in hepatocytes, which promotes hedgehog (Hh) ligand production in stellate cells, leading to the activation of Hh signaling in hepatocytes and consequent cell proliferation. Collectively, our study identified miR-182-5p as a critical regulator of LR and uncovers a Cyp7a1/cholic acid-dependent mechanism by which hepatocytes crosstalk to stellate cells to facilitate LR.

2022-08-10 | GSE206451 | GEO

Expression data from the hepatic stellate cell line LX-2 after treatment with DMOG and from the liver sinusoidal endothelial cell line TRP3 after incubation with conditioned medium of DMOG-treated LX-2

Project description:Expression data from the hepatic stellate cell line LX-2 after treatment with the prolylhydroxylase inhibitor dimethyloxalylglycine (DMOG) and from the liver sinusoidal endothelial cell line TRP3 after incubation with conditioned medium of DMOG-treated LX-2 Prolyl-hydroxylase inhibitors such as dimethyloxalylglycine (DMOG) stabilize HIF-1α, thereby chemically inducing hypoxia, which also accelerates liver volume increase when given with portal rerouting. We used microarrays to clarify the cellular crosstalk of the different cell types in accelerated liver regeneration by examining the role of hepatic stellate cells (HSC) and liver sinusoidal endothelial cells (LSEC).

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The effect of postoperative stellate ganglion block on myocardial injury in patients undergoing laparoscopic radical resection of colorectal cancer

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Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation

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ZNF341 controls STAT3 expression and thereby immunocompetence

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CBC-ARS2 stimulates 3'-end maturation of multiple RNA families and favors cap-proximal processing

Project description:The nuclear cap-binding complex (CBC) stimulates multiple steps in several RNA maturation pathways, but how it functions in humans is incompletely understood. For small capped RNAs like pre-snRNAs, the CBC recruits PHAX. Here, we identify the CBCAP complex, composed of CBC, Ars2 and PHAX, and show that both CBCAP and CBC-Ars2 complexes can be reconstituted from recombinant proteins. Ars2 stimulates PHAX binding to the CBC as well as snRNAs 3'-end processing, hereby coupling maturation with export. In vivo, CBC and Ars2 bind similar capped non-coding and coding RNAs, and stimulate their 3M-bM-^@M-^Y-end processing. Strongest effects are displayed for cap-proximal polyadenylation sites, thereby favoring premature transcription termination. Ars2 functions in part through the mRNA 3M-bM-^@M-^Y-end cleavage factor CLP1, which binds RNA Polymerase II through PCF11. Ars2 is thus a major CBC effector that stimulates functional and cryptic 3'-end processing sites. In total 12 samples; 4 control IP, 2 Flag- Ars2 IP and 2 Flag-CBP20 IP; 2 control FFL siRNA and 2 siRNA Ars2

2013-11-08 | E-GEOD-52131 | biostudies-arrayexpress

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