Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1034241 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26623709_1.fastq.gz | Fastqsanger.gz | |||
| SRR26623709_2.fastq.gz | Fastqsanger.gz | |||
| SRR26623710_1.fastq.gz | Fastqsanger.gz | |||
| SRR26623710_2.fastq.gz | Fastqsanger.gz | |||
| SRR26623711_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Liver fibrosis has been implicated in the pathogenesis of various liver disease. Thus far, there is still no effective intervention means for this process. Recently, we have demonstrated that S100A16 participated in liver lipid accumulation and renal fibrosis. Therefore, we hypothesized that S100A16 took a critical role in liver fibrosis. S100a16 transgenic and knockdown mice were generated and stimulated with carbon tetrachloride, bile duct ligation and methionine choline deficiency diet. Alterations of gene expression in hepatic stellate cells from wild type and S100a16+/- mice were investigated by transcriptome sequencing. S100A16 expression levels in liver tissue of patients and rodent models of liver fibrosis were markedly increased. S100a16 transgenic mice showed spontaneous liver fibrosis after normal feeding for 6 months. On the contrary, silencing of S100a16 exhibited obvious protective effect against liver fibrosis caused by different stimulations. Meanwhile, results showed that deletion of S100a16 significantly inhibited hepatic stellate cells (HSCs) activation cultured in fetal bovine serum contained medium. RNA sequencing results revealed that mechanistically, C-X-C motif chemokine receptor 4 (Cxcr4) participated in the process of S100a16 in liver fibrosis. Knockdown of S100a16 inhibited Cxcr4 expression through augmenting P53 expression. SDF-1α/CXCR4-dependent extracellular signal-regulated kinase 1/2 and Akt phosphorylation mediated the effects of S100a16 on α-smooth muscle actin expression and HSCs activation. These data indicate that S100a16 deficiency prevents liver fibrosis by inhibiting Cxcr4 expression. Targeting S100A16 may provide insights into the pathogenesis of liver fibrosis and pave the way for developing strategies for liver fibrosis-related diseases prevention and treatment.
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Project description:Angiocrine signaling by liver sinusoidal endothelial cells (LSEC) regulates liver functions such as liver growth, metabolic maturation, and regeneration. Recently, we identified GATA4 as the master regulator of LSEC specification during development. Here, we studied endothelial GATA4 in the adult liver and in hepatic disease pathogenesis. We generated adult Clec4g-icretg/0xGata4fl/fl (Gata4LSEC KO) mice with deficiency of Gata4 in LSEC. Livers were analyzed by histology, electron microscopy, immunohistochemistry/immunofluorescence, in-situ hybridization, and by expression profiling and ATAC-sequencing of isolated LSEC. For liver regeneration, partial hepatectomy was performed. As models of liver fibrosis, CDAA diet and chronic CCl4 exposure were applied. Human single cell RNAseq data sets were analyzed for endothelial alterations in healthy and cirrhotic livers. Genetic Gata4 deficiency in LSEC in adult mice caused perisinusoidal liver fibrosis, hepatopathy and impaired liver regeneration. Sinusoidal capillarization and LSEC-to-continuous endothelial transdifferentiation were accompanied by a profibrotic angiocrine switch including de novo endothelial expression of hepatic stellate cell-activating cytokine PDGFB. Increased chromatin accessibility and amplification by activated Myc mediated angiocrine PDGFB expression. In CDAA diet-induced perisinusoidal liver fibrosis, LSEC showed repression of GATA4, activation of MYC and the profibrotic angiocrine switch already detected in Gata4LSEC KO mice. Comparison of CDAA-fed Gata4LSEC KO and control mice demonstrated that endothelial Gata4 indeed protects from dietary-induced perisinusoidal liver fibrosis. In human cirrhotic livers, Gata4-positive LSEC and endothelial Gata4 target genes were reduced, while non-LSEC endothelial cells and Myc target genes including PDGFB were enriched. Endothelial GATA4 protects from perisinusoidal liver fibrosis by repressing MYC activation and profibrotic angiocrine signaling on the chromatin level. Therapies targeting the GATA4/MYC/PDGFB/PDGFRβ axis offer a promising strategy for the prevention and treatment of liver fibrosis.
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Project description:Purpose: The goal of this study is to investigate the effect of recombinant human Cytoglobin (rhCYGB) on liver fibrosis induced by TAA in mice. Method: mRNA profiles of liver tissues from TAA-control mice and TAA-rhCYGB treated mice were generated by deep sequencing. Results: The RNA-seq data confirmed that extracellular matrix-encoding genes and fibrosis-related genes were down-regulated by the rhCYGB treatment.
2020-08-25 | GSE156777 | GEO