Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative ATAC-seq of cultured mouse Acta2-R179C aortic SMCs versus healthy controls

ABSTRACT: Comparative ATAC-seq of cultured mouse Acta2-R179C aortic SMCs versus healthy controls

PROVIDER: PRJNA1006310 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25663031_1.fastq.gz	Fastqsanger.gz
	SRR25663031_2.fastq.gz	Fastqsanger.gz
	SRR25663032_1.fastq.gz	Fastqsanger.gz
	SRR25663032_2.fastq.gz	Fastqsanger.gz
	SRR25663033_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Comparative ATAC-seq of cultured mouse Acta2-R179C aortic SMCs versus healthy controls

Project description:Explanted aortic SMCs from transgenic,Acta2-R179C/+ mice and littermate controls were cultured and subjected to assay for transposase accessible chromatin by sequencing (ATAC-seq) to determine how the R179C variant influences chromatin accessibility.

2023-08-17 | GSE241055 | GEO

Aortic single-cell RNA sequencing in ACTA2 R179 variants

Project description:Single-cell RNA datasets for aortic tissue from 8-week-old inducible smooth muscle cell-specific knock-in of Acta2 R179C mutation vs. littermate controls and aortic aneurysm tissue from a human patient carrying an ACTA2 R179H variant vs. a pediatric organ donor healthy control.

2023-01-01 | GSE201091 | GEO

MicroRNA transcriptional profiling in serum-starved human aortic smooth muscle cells

Project description:We sought to identify microRNAs that were differentially regulated in cultured primary human aortic smooth muscle cells (SMCs) when exposed to growth arrest via serum starvation over two time points - 48 hours and 72 hours, when compared with serum-fed cells. This treatment leads to increased expression of SMC differentiation markers such as ACTA2, MYH11 and TAGLN. We identified 31 significantly regulated miRNA candidates during this process, 28 rising and 3 falling. Human aortic SMCs (AoSMCs) were propagated in growth media. Control plates were harvested, and the remaining plates were serum starved for 48 (SS48) or 72 hours (SS72) in serum-free basal media. Several arrays were excluded from final analysis after QC, resulting in a final set of 10.

2009-12-25 | E-GEOD-19544 | biostudies-arrayexpress

MicroRNA transcriptional profiling in serum-starved human aortic smooth muscle cells

2009-12-25 | GSE19544 | GEO

Aortic single-cell RNA sequencing in ACTA2 R179 variants

Project description:Aortic single-cell RNA sequencing in ACTA2 R179 variants

| PRJNA828323 | ENA

Cholesterol and TNF-induced transcriptomic changes in Mus musculus aortic smooth muscle cells

Project description:To map gene regulation downstream of cholesterol overload and NF-kappaB signaling in smooth muscle cells (SMCs), we cultured primary aortic SMCs from wildtype mice with cyclodextrin-complexed cholesterol or the prototypical NF-kappaB activator, tumor necrosis factor (TNF), or both.

2023-05-29 | E-MTAB-12069 | biostudies-arrayexpress

Nuclear Factor-kappa B inhibition in mouse aortic smooth muscle cells stimulated by cholesterol overload or tumor necrosis factor

Project description:To test whether cholesterol overload in smooth muscle cells (SMCs) drives NF-kappaB signaling and to map target genes controlled by NF-kappaB signaling in SMCs, we cultured primary aortic SMCs from wildtype mice in the presence of cyclodextrin-complexed cholesterol or the prototypical NF-kappaB activator tumor necrosis factor (TNF) with or without blocking canonical NF-kappaB signaling by knockdown of inhibitor of kappaB kinase beta (Ikbkb).

2023-12-07 | E-MTAB-13416 | biostudies-arrayexpress

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

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

2023-09-05 | GSE233625 | GEO

Fibroblast SPP1 mediates ECM deposition and inhibits SMC contractility in MFS aortic aneurysm

Project description:Mutations in the Fbn1 gene cause Marfan Syndrome (MFS) and are associated with excessive transforming growth factor beta (TGF-β) signalling activation, which contributes to extracellular matrix (ECM) homeostasis disruption, thoracic aortic aneurysm (TAA) and dissection development. In this study, we aimed to explore the underlying events contributing to ECM metabolism imbalance and TAA and dissection formation in MFS. We performed sequencing analysis and investigated differentially expressed genes as well as cellular communication using CellChat. Fourteen ECM-related differentially expressed genes (DEGs) were identified. Among the 14 genes, secreted phosphoprotein 1 (Spp1) was involved in multiple pathological processes. We then stimulated primary mouse perivascular fibroblasts and aortic SMCs with recombinant Spp1 and recorded increased collagen expression in fibroblasts and decreased expression of Acta2 and Tagln in SMCs. We also investigated SPP1 levels in healthy controls and patients with TAA and found that elevated SPP1 levels were associated with an increased risk of TAA. Our results have indicated that Spp1 regulates ECM changes in fibroblasts and SMCs contractility during TAA. We believe that our study makes a significant contribution to the literature because our results suggest that Spp1 may serve as a potential target for TAA treatment.

2024-12-12 | GSE190720 | 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