Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Endothelial TGFβ signaling drives vascular inflammation and atherosclerosis [scRNA-Seq]

ABSTRACT: Endothelial TGFβ signaling drives vascular inflammation and atherosclerosis [scRNA-Seq]

PROVIDER: PRJNA555594 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9718660_1.fastq.gz	Fastqsanger.gz
	SRR9718660_2.fastq.gz	Fastqsanger.gz
	SRR9718670_1.fastq.gz	Fastqsanger.gz
	SRR9718670_2.fastq.gz	Fastqsanger.gz
	SRR9718661_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Endothelial TGFβ signaling drives vascular inflammation and atherosclerosis [scRNA-Seq]

Project description:Endothelial TGFβ signaling is one of the primary drivers of atherosclerosis-associated vascular inflammation. Inhibition of endothelial TGFβ signaling in hyperlipidemic mice reduces vessel wall inflammation and vascular permeability and leads to arrest of disease progression and regression of established lesions. We performed scRNAseq method to examine endothelial cell gene expression profile using Apoe and EC specific TGFbR1/2 KO in Apoe background mice.

2019-08-26 | GSE134557 | GEO

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis [ChIP-Seq]

2019-08-26 | GSE134556 | GEO

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis [bulk RNA-Seq]

2019-08-26 | GSE134555 | GEO

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis

Project description:Endothelial TGFb signaling drives vascular inflammation and atherosclerosis

| PRJNA555585 | ENA

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis [ChIP-Seq]

Project description:Endothelial TGFb signaling drives vascular inflammation and atherosclerosis [ChIP-Seq]

| PRJNA555593 | ENA

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis [bulk RNA-Seq]

Project description:Endothelial TGFb signaling drives vascular inflammation and atherosclerosis [bulk RNA-Seq]

| PRJNA555592 | ENA

Endothelial IGFBP6 Suppresses Vascular Inflammation and Atherosclerosis

Project description:Endothelial IGFBP6 Suppresses Vascular Inflammation and Atherosclerosis

| PRJNA1104204 | ENA

Endothelial TGF-β signalling drives vascular inflammation and atherosclerosis.

Project description:Atherosclerosis is a progressive vascular disease triggered by interplay between abnormal shear stress and endothelial lipid retention. A combination of these and, potentially, other factors leads to a chronic inflammatory response in the vessel wall, which is thought to be responsible for disease progression characterized by a buildup of atherosclerotic plaques. Yet molecular events responsible for maintenance of plaque inflammation and plaque growth have not been fully defined. Here we show that endothelial TGFβ signaling is one of the primary drivers of atherosclerosis-associated vascular inflammation. Inhibition of endothelial TGFβ signaling in hyperlipidemic mice reduces vessel wall inflammation and vascular permeability and leads to arrest of disease progression and regression of established lesions. These pro-inflammatory effects of endothelial TGFβ signaling are in stark contrast with its effects in other cell types and identify it as an important driver of atherosclerotic plaque growth and show the potential of cell-type specific therapeutic intervention aimed at control of this disease.

| S-EPMC6767930 | biostudies-literature

JAG1-NOTCH4 mechanosensing drives atherosclerosis

Project description:Endothelial cell (EC) sensing of fluid shear stress regulates atherosclerosis, a disease of arteries that causes heart attack and stroke. Atherosclerosis preferentially develops at regions of arteries exposed to low oscillatory shear stress (LOSS), whereas high shear regions are protected. We show using inducible EC-specific genetic deletion in hyperlipidaemic mice that the Notch ligands JAG1 and DLL4 have opposing roles in atherosclerosis. While endothelial Jag1 promoted atherosclerosis at sites of LOSS, endothelial Dll4 was atheroprotective. Analysis of porcine and murine arteries and cultured human coronary artery EC exposed to experimental flow revealed that JAG1 and its receptor NOTCH4 are strongly upregulated by LOSS. Functional studies in cultured cells and in mice with EC-specific deletion of Jag1 show that JAG1-NOTCH4 signalling drives vascular dysfunction by repressing endothelial repair. These data demonstrate a fundamental role for JAG1-NOTCH4 in sensing LOSS during disease, and suggest therapeutic targeting of this pathway to treat atherosclerosis.

2022-09-06 | GSE206117 | GEO

Ligustilide targets SMAD3, obstructing vascular fibrosis process in preventing atherosclerosis

Project description:Atherosclerosis is a persistent inflammatory state accompanied by lipid overload. Vascular fibrosis is one of the primary causes of atherosclerosis development. Although ligustilide (Lig) was shown to exert obvious antiatherogenic effects in previous studies, its precise mechanism has not been comprehensively discussed. In this paper, pharmacologic studies were performed to explore the pharmacodynamic effects of Lig on protecting aorta vascular wall structures and modulating serum inflammatory factors in ApoE-/- mice. Chemical proteomics based on a Lig-derived photoaffinity labelling (Lig-PAL) probe were applied to identify potential therapeutic targets. Mothers against decapentaplegic homologue 3 (SMAD3), which is closely related to the development of vascular fibrosis and atherosclerosis, was identified as a potential target of Lig. Lig suppressed the phosphorylation and nuclear translocation of SMAD3 by blocking the interaction between SMAD3 and transforming growth factor-β (TGF-β) receptor 1, thereby inhibiting the collagen synthesis process, preventing vascular fibrosis and improving atherosclerosis. The quantitative proteomics results from Lig-treated atherosclerotic ApoE-/- mice also indicated that Lig inhibits the expression of collagens I and III, interferes with collagen fibril organization processes and protects the aorta from vascular fibrosis. Hence, developing a novel SMAD3 inhibitor may present another therapeutic option for preventing atherosclerosis.

2020-01-21 | PXD017125 | Pride

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