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Single-cell analysis of whole hepatic non-parenchymal cells from normal and CCl4-injured mice

ABSTRACT: Single-cell analysis of whole hepatic non-parenchymal cells from normal and CCl4-injured mice

PROVIDER: PRJNA553529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9659728.fastq.gz	Fastqsanger.gz
	SRR9659729.fastq.gz	Fastqsanger.gz

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Single-cell analysis of whole hepatic non-parenchymal cells from normal and CCl4-injured mice

Project description:This study used 10X Genomics, single-cell RNA-sequencing to examine the heterogeneity of liver non-parenchymal cell types present in the normal and CCl4-mediated fibrotic mice.

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Transcriptional profiling of hepatic stellate cells (HSCs) isolated from Western diet/high fructose-fed C57BL6/J mice, carbon tretrachloride (CCl4)-treated C57BL6/J mice, and of murine HSCs differentiated in vitro

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Phenotype and function of ex vivo expanded liver progenitor-like cells through liver parenchymal and non-parenchymal reversion

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Normal and injured liver sinusoidal endothelial cells

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Expression data from murine hepatic stellate cells

Project description:Wnt/β-catenin is involved in every aspect of embryonic development and in the pathogenesis of many human diseases, and is also implicated in organ fibrosis. However, the role of β-catenin-mediated signaling on liver fibrosis remains unclear. To explore this issue, the effects of PRI-724, a selective inhibitor of the cAMP-response element-binding protein-binding protein (CBP)/β-catenin interaction, on liver fibrosis were examined using carbon tetrachloride (CCl4)- or bile duct ligation (BDL)-induced mouse liver fibrosis models. Following repetitive CCl4 administrations, the nuclear translocation of β-catenin was observed only in the non-parenchymal cells in the liver. PRI-724 treatment reduced the fibrosis induced by CCl4 or BDL, accompanied by the suppression of S100A4 expression, a CBP/β-catenin transcript. C-82, an active form of PRI-724, inhibited the activation of isolated primary mouse quiescent hepatic stellate cells (HSCs) and promoted cell death in culture-activated HSCs. During the fibrosis resolution period, an increase in F4/80+ CD11b+ and Ly6Clow CD11b+ macrophages was induced by CCl4 and was sustained for two weeks thereafter, even after having stopped CCl4 treatment. PRI-724 accelerated the resolution of CCl4-induced liver fibrosis, and this was accompanied by increased matrix metalloproteinase (MMP)-9, MMP-2, and MMP-8 expression in intrahepatic leukocytes. These results suggest that the inhibition of CBP/β-catenin suppresses liver fibrosis through the inhibition of HSCs activation, the induction of activated HSC death, and the production of MMPs from macrophages. Thus, targeting the CBP/β-catenin interaction may become a new therapeutic strategy in treating liver fibrosis. We used microarrays to detail the global change of gene expression by PRI-724 (C-82)-treatment in culture-activated murine hepatic stellate cells.

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