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Transcriptomic profiling of liver sinusoidal endothelial cells during chronic liver disease reveals stage-specific secretory signature

ABSTRACT: Transcriptomic profiling of liver sinusoidal endothelial cells during chronic liver disease reveals stage-specific secretory signature

PROVIDER: PRJNA691975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13433962.fastq.gz	Fastqsanger.gz
	SRR13433963.fastq.gz	Fastqsanger.gz
	SRR13433964.fastq.gz	Fastqsanger.gz
	SRR13433965.fastq.gz	Fastqsanger.gz
	SRR13433966.fastq.gz	Fastqsanger.gz

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Rat transcriptomic profiling of liver sinusoidal endothelial cells during chronic liver disease reveals stage-specific secretory signature

Project description:Rat transcriptomic profiling of liver sinusoidal endothelial cells during chronic liver disease reveals stage-specific secretory signature

| PRJNA692264 | ENA

Transcriptomic profiling of liver sinusoidal endothelial cells during chronic liver disease reveals stage-specific secretory signature

Project description:In this study RNAseq was used for studying the transcriptome profile of primary liver sinusoidal endothelial cells (LSECs) isolated from non-lesioned non-tumorous liver tissues (considered as healthy) and from cirrhotic liver explants (ethanol etiology). Results showed different transcriptomic profile between two populations of LSECs with 1374 significant deregulated genes (fold-change>1.5 and p-vale<0.05) in cirrhotic-LSECs compared with healthy-LSECs.

2021-09-24 | GSE164799 | GEO

Rat transcriptomic profiling of liver sinusoidal endothelial cells during chronic liver disease reveals stage-specific secretory signature

Project description:RNAseq was applied to define the transcriptome of primary LSECs from rats with acute liver injury, mild liver fibrosis and advanced chronic liver disease (CLD) (due to CCl4 or thioacetamide administration). Results showed different transcriptomic profile during progression of CLD, and a large number of significant de-regulated genes (1412) were shared in cirrhotic CCl4- and TAA-LSECs (fold-change>1.5 and p-vale<0.05)compared with their respective healthy-LSECs.

2021-09-24 | GSE164878 | GEO

Transcriptomic Profiling of the Liver Sinusoidal Endothelium during Cirrhosis Reveals Stage-Specific Secretory Signature.

Project description:The poor prognosis of chronic liver disease (CLD) generates the need to investigate the evolving mechanisms of disease progression, thus disclosing therapeutic targets before development of clinical complications. Considering the central role of liver sinusoidal endothelial cells (LSECs) in pre-neoplastic advanced CLD, the present study aimed at investigating the progression of CLD from an endothelial holistic perspective. RNAseq defined the transcriptome of primary LSECs isolated from three pre-clinical models of advanced CLD, during the progression of the disease, and from fresh human cirrhotic tissue. At each stage of the disease, the effects of LSECs secretome on neighboring cells and proteomic analysis of LSECs-derived extracellular vesicles (EVs) were also determined. CLD was associated with deep common modifications in the transcriptome of LSECs in the pre-clinical models. Pathway enrichment analysis showed predominance of genes related with pro-oncogenic, cellular communication processes, and EVs biogenesis during CLD progression. Crosstalk experiments revealed endothelial EVs as potent angiocrine effectors. The proteome of LSECs EVs showed stage-specific signatures, including over-expression of tropomyosin-1. Proof-of-principle experiments treating cirrhotic HSCs with recombinant tropomyosin-1 suggested de-activating effects. Our data provide the basis for discovering novel biomarkers and therapeutic targets for new disease-modifying treatments for patients with advanced CLD.

| S-EPMC8198220 | biostudies-literature

Normal and injured liver sinusoidal endothelial cells

Project description:Comparison of C57BL/6J 8-10 weeks male mouse liver sinusoidal endothelial cells (LSEC) from normal liver and from liver injured by carbon tetrachloride administration. Keywords: other

2004-10-01 | E-GEOD-1689 | biostudies-arrayexpress

Molecular atlas of fetal and adult human liver sinusoidal endothelial cells: a F8 secreting cell [methylation III]

Project description:In-silico analysis to identify molecular signature of liver sinusoidal endothelial cells in comparison to other endohtelial cells

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Normal and injured liver sinusoidal endothelial cells

2004-10-01 | GSE1689 | GEO

Analysis of Scavenger-Receptor Type H deficient liver sinusoidal endothelial cells

Project description:Two of the most highly abundant transcripts in liver sinusoidal endothelial cells are Stab1 and Stab2, we investigated downstream effects on liver sinusoidal endothelial cells by disrupting their expression. We used microarrays to detail the global programme of gene expression in liver sinusoidal endothelial cells deficient for Scavenger-Receptor type H compared to Wildtype.

2021-10-11 | GSE157900 | GEO

Aging-associated transcriptome changes in liver sinusoidal endothelial cells.

Project description:Aging-associated transcriptome changes in liver sinusoidal endothelial cells. RNA was prepared from liver sinusoidal endothelial cells of the male 8 weeks and 24 months old C57BL/6J mice.RNA samples were then subjected to RNA-sequencing and gene expression profiling analysis.

2022-10-29 | GSE216592 | GEO

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.

2024-01-01 | GSE233284 | GEO

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