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Blocking the activation of TGFβ signaling in liver sinusoidal endothelial cells alleviates liver fibrosis in mice

ABSTRACT: Blocking the activation of TGFβ signaling in liver sinusoidal endothelial cells alleviates liver fibrosis in mice

PROVIDER: PRJNA996947 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25373416_1.fastq.gz	Fastqsanger.gz
	SRR25373416_2.fastq.gz	Fastqsanger.gz
	SRR25373417_1.fastq.gz	Fastqsanger.gz
	SRR25373417_2.fastq.gz	Fastqsanger.gz
	SRR25373418_1.fastq.gz	Fastqsanger.gz

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Blocking the activation of TGFβ signaling in liver sinusoidal endothelial cells alleviates liver fibrosis in mice

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Project description:In this work, the effect of splenectomy on liver sinusoidal cells was studied. For this purpose in the animals were reproduced splenectomy, and after 7 days 70% liver resection was performed. Animals in which the spleen was intact and only 70% liver resection was performed served as a comparison group. Animals in which only the spleen was removed also served as controls. The animals were removed from the experiment after 24 hours, 3 and 7 days. Liver sinusoidal cells were isolated from the livers of control animals as well as from the liver after 70% resection by magnetic sorting using the CD146 beads. RNA was isolated from the obtained liver sinusoidal cells and used for transcriptome analysis. Liver sinusoidal cells in the regenerating liver were transcriptomically enriched for signaling pathways associated with monocyte migration, cell adhesion and cell death.

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H3K27ac profiling in liver sinusoidal endothelial cells through chromatin immunoprecipitation and sequencing

Project description:Portal hypertension (PHTN) is a severe complication of liver cirrhosis. It is associated with intrahepatic sinusoidal remodeling induced by sinusoidal resistance and angiogenesis. Collagen type IV (COL4), a major component of basement membrane (BM), forms in liver sinusoids upon chronic liver injury. However, the cellular source and transcriptional regulation of COL4, as well as how it progresses in liver diseases is unknown. Here, we examined how COL4 is produced and how it regulates sinusoidal remodeling in PHTN. RNA-seq analysis on human cirrhotic livers revealed an increase in COL4 expression, which was further confirmed via immunofluorescence (IF) staining. scRNA-seq analysis identified Liver sinusoidal endothelial cells (LSECs) as the predominant source of COL4 expression in mouse liver, which was upregulated in a TNFα-NFκB dependent manner. Epigenetic repression of enhancer-promoter interaction silences COL4 gene expression via dCas9-KRAB-mediated epigenome editing approach. LSEC-specific COL4 mutation or repression abrogated sinusoidal resistance and angiogenesis, thereby alleviated sinusoidal remodeling and PHTN. Our findings reveal LSECs as a major source of COL4 in the liver which plays a prominent role in sinusoidal remodeling and PHTN.

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