Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNA-seq of Lineage-tracing Mice Identifies Smooth Muscle Cell Phenotypic Alterations in Aortic Aneurysms and Dissections

ABSTRACT: ScRNA-seq of Lineage-tracing Mice Identifies Smooth Muscle Cell Phenotypic Alterations in Aortic Aneurysms and Dissections

PROVIDER: PRJNA975573 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24710504_1.fastq.gz	Fastqsanger.gz
	SRR24710504_2.fastq.gz	Fastqsanger.gz
	SRR24710505_1.fastq.gz	Fastqsanger.gz
	SRR24710505_2.fastq.gz	Fastqsanger.gz
	SRR24710506_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

Smooth muscle cell reprogramming in aortic aneurysms

Project description:Smooth muscle cell reprogramming in aortic aneurysms

| PRJNA591801 | ENA

Smooth muscle cell reprogramming in aortic aneurysms [scRNA-Seq]

Project description:Smooth muscle cell reprogramming in aortic aneurysms [scRNA-Seq]

| PRJNA591808 | ENA

Smooth muscle cell reprogramming in aortic aneurysms [RNA-Seq]

Project description:Smooth muscle cell reprogramming in aortic aneurysms [RNA-Seq]

| PRJNA591577 | ENA

ScRNA-seq of Sting-KO Mice Identifies Smooth Muscle Cell Phenotypic Alterations in Aortic Aneurysms and Dissections

Project description:ScRNA-seq of Sting-KO Mice Identifies Smooth Muscle Cell Phenotypic Alterations in Aortic Aneurysms and Dissections

| PRJNA976930 | ENA

Smooth muscle cell reprogramming in aortic aneurysms [RNA-Seq]

Project description:Smooth muscle cell TGFβ signaling is one of the primary drivers of smooth muscle cell maturation. Inhibition of smooth muscle cell TGFβ signaling in hyperlipidemic mice induces vessel wall inflammation and vessel wall dilation/dissection and leads aortic aneurysm. We performed bulk RNAseq method to examine smooth muscle cell gene expression profile using fresh human tissues from normal aortic media smooth muscle cells and aneurysm aortic media smooth muscle cells.

2020-03-01 | GSE140947 | GEO

Notch1 haploinsufficiency causes aortic aneurysms in mice

Project description:Ascending aortic aneurysms (AscAA) are a life-threatening disease whose molecular basis is poorly understood. Mutations in NOTCH1 have been linked to bicuspid aortic valve (BAV), which is associated with AscAA. Here, we describe a novel role for Notch1 in AscAA. We found that Notch1 haploinsufficiency exacerbated the aneurysmal aortic root dilation seen in the Marfan syndrome mouse model and that heterozygous deletion of Notch1 in the second heart field (SHF) lineage recapitulated this exacerbated phenotype. Lineage tracing analysis showed that loss of Notch1 in the SHF reduces the number of SHF-derived smooth muscle cells in the aortic root, and RNA-seq analysis demonstrated distinct in vivo expression patterns between lineage-specific regions of the ascending aorta. Finally, Notch1+/- mice in a predominantly 129S6 background develop aortic root dilation, indicating that loss of Notch1 independently predisposes to AscAA. These findings are the first to demonstrate a SHF lineage-specific role for Notch1 in AscAA and suggest that genes linked to the development of BAV may also contribute to the associated aortopathy.

2017-09-29 | GSE104365 | GEO

ScRNA-seq of Lineage-tracing Mice Identifies Smooth Muscle Cell Phenotypic Alterations in Aortic Aneurysms and Dissections

Project description:ScRNA-seq analysis revealed that aortic stress induced the transition of SMCs from a primary contractile phenotype to proliferative, extracellular matrix (ECM)-producing, inflammatory, and dying phenotypes. Lineage tracing showed the complete transformation of SMCs to fibroblasts and macrophages. ScATAC-seq analysis indicated that these phenotypic alterations were controlled by chromatin remodeling marked by the reduced chromatin accessibility of contractile genes and the induced chromatin accessibility of genes involved in ECM, inflammation, and cell death. IRF3, a pro-inflammatory transcription factor activated by cytosolic DNA, was identified as a key driver for the transition of aortic SMCs from a contractile phenotype to an inflammatory phenotype. In cultured SMCs, cytosolic DNA signaled through its sensor STING-TBK1 to activate IRF3, which bound and recruited EZH2 to contractile genes to induce repressive H3K27me3 modification and contractile gene suppression. In contrast, dsDNA-STING-IRF3 signaling induced inflammatory gene expression in SMCs. In Sting-/- mice, the aortic stress–induced transition of SMCs into an inflammatory phenotype was prevented, and SMC populations were preserved. Finally, profound SMC phenotypic alterations in diverse directions were detected in human ATAAD tissues.

2023-09-05 | GSE233257 | GEO

NHLBI GO-ESP: Family Studies (Thoracic aortic aneurysms leading to acute aortic dissections)

Project description:NHLBI GO-ESP: Family Studies (Thoracic aortic aneurysms leading to acute aortic dissections)

| PRJNA75309 | ENA

Smooth muscle cell reprogramming in aortic aneurysms [scRNA-Seq]

Project description:Smooth muscle cell TGFβ signaling is one of the primary drivers of smooth muscle cell maturation. Inhibition of smooth muscle cell TGFβ signaling in hyperlipidemic mice induces vessel wall inflammation and vessel wall dilation/dissection and leads aortic aneurysm. We performed scRNAseq method to examine smooth muscle cell gene expression profile using Apoe and SMC specific TGFbR2 KO in Apoe background mice.

2020-03-01 | GSE141031 | GEO

Profile of macrophages in human abdominal aortic aneurysms: a transcriptomic, proteomic and antibody protein array study

Project description:Abdominal aortic aneurysms (AAA), are defined by an increased aortic diameter and characterized by impairment of the extracellular matrix, macrophages infiltration and decreased density of smooth muscle cells. Our aim is to identify the key molecules involved in the pathogenesis of AAAs. This study investigated transcriptomic and proteomic profiles of macrophages from AAA patients (> 50 mm aortic diameter) and peripheral arterial occlusion (PAO) patients without AAA detected, who both needed a surgery.

2010-05-12 | GSE21803 | GEO

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