Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 12

Similar Datasets

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

Project description:Purpose: To detect the alterations in transcriptional profile of primary LSECs isolated from Tgfbr2 ECKO mice and Tgfbr2f/f mice in CCl4-induced liver fibrosis.

2023-07-27 | GSE237859 | GEO

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

Blocking hyaluronan synthesis alleviates acute lung allograft rejection.

Project description:Blocking hyaluronan synthesis alleviates acute lung allograft rejection.

| PRJNA759258 | ENA

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

VEGF-A stimulated gene expression in human liver sinusoidal endothelial cells

Project description:Transcriptomic analysis of VEGF-A stimulated liver sinusoidal endothelial cell gene expression. Untreated cells were compared to those treated with VEGF-A. VEGF-A stimulation is critical for normal LSEC phenotype, and the response to liver injury Two conditions: untreated vs. VEGF-A treated. LSEC from 2 donors were pooled. 4 technical repeats.

2013-06-01 | E-GEOD-41110 | biostudies-arrayexpress

Expression data from fatty acid and bile acid receptor agonist treated liver sinusoidal endothelial cells

Project description:Liver sinusoidal endothelial cells (LSEC) are unique endothelial cell typelining the sinusoids of the liver and we have shown that these cells respond in a unique matter when exposed to saturated and unsaturated free fatty acids (FFA) and bile acids. We used microarray to analyze the transcriptional differences between the LSEC exposed to free fatty acids and bile acid receptor agonists to further shed light on their role in non-alcoholic fatty liver disease. The Murine Liver Sinusoidal Endothelial Cell Line (TSEC) was treated with palmitic and oleic acid or the bile acid receptor agonist INT-767 for 8 hours. Total RNA was then harvested to determine transcriptional differences.

2015-05-07 | E-GEOD-67651 | biostudies-arrayexpress

Comparison of gene expression between Human umbilical vein endothelial cells and Human liver sinusoidal endothelial cells

Project description:To identify leukocyte adhesion receptors which differentially regulate recruitment in human liver sinusoidal endothelial cells compared to a protoptypic venular endothelium Gene expression was measured in four groups Group 1: cultured human liver sinusoidal endothelial cells (HSEC) Group 2: cultured human umbilical vein endothelial cells (HUVEC) Group3: Interferon gamma and tumour necrosisfactor alpha treated HSEC and Group 4: Interferon gamma and tumour necrosisfactor alpha treated HUVEC. Two replicates were used for each group.

2016-10-24 | E-GEOD-78020 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data