Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of depletion of LEMD3 on chromatin accessibility of A7r5 vascular smooth muscle cells [Hi-C]

ABSTRACT: The contractile phenotype of vascular smooth muscle cells is essential for maintaining vascular homeostasis.In this study, we found that LEMD3, a nuclear membrane protein, may be involved in maintaining the contractile phenotype of vascular smooth muscle cells through a genome-scale CRISPR screen. Mechanistically, we combined RNA-seq with ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to find out differentially expressed genes and altered chromatin accessibility. By overlapping down-regulated genes and genes located in less accessible chromatin regions, we identified 143 genes including VSMCs contractile genes such as Acta2, Cnn1, Tagln, and key transcription factor Srf, suggesting that LEMD3 maintains VSMCs contractile phenotype by regulating chromatin accessibility.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE263853 | GEO | 2025/04/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of depletion of LEMD3 on chromatin accessibility of A7r5 vascular smooth muscle cells [ATAC-seq]

Project description:The contractile phenotype of vascular smooth muscle cells is essential for maintaining vascular homeostasis.In this study, we found that LEMD3, a nuclear membrane protein, may be involved in maintaining the contractile phenotype of vascular smooth muscle cells through a genome-scale CRISPR screen. Mechanistically, we combined RNA-seq with ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to find out differentially expressed genes and altered chromatin accessibility. By overlapping down-regulated genes and genes located in less accessible chromatin regions, we identified 143 genes including VSMCs contractile genes such as Acta2, Cnn1, Tagln, and key transcription factor Srf, suggesting that LEMD3 maintains VSMCs contractile phenotype by regulating chromatin accessibility.

2025-04-01 | GSE263815 | GEO

Effect of depletion of LEMD3 on gene expression of A7r5 vascular smooth muscle cells [RNA-seq]

2025-04-01 | GSE263053 | GEO

Effect of depletion of LEMD3 on histone modification H3K27ac of A7r5 vascular smooth muscle cells [ChIP-seq]

2025-04-01 | GSE263052 | GEO

Phenotype modulation of VSMCs on patterned substrate

Project description:Loss of contractility and acquisition of an epithelial phenotype of vascular smooth muscle cells (VSMCs) are key events in proliferative vascular pathologies such as atherosclerosis and post-angioplastic restenosis. There is no proper cell culture system allowing VSMC differentiation so that it is difficult to delineate the molecular mechanism responsible for proliferative vasculopathy. We investigated whether a micro-patterned substrate could restore the contractile phenotype of VSMCs in vitro. To induce and maintain the differentiated VSMC phenotype in vitro, we introduced a micro-patterned groove substrate to modulate the morphology and function of VSMCs.

2013-11-14 | E-MTAB-1888 | biostudies-arrayexpress

The effect of Schisandra chinensis fruit extract (SCE) and Schisandrin B (SchB) on gene expression profile in TGF-β1-treated A7r5 rat aortic smooth muscle cell

Project description:Schisandra chinensis fruit extract (SCE) and its active ingredient Schisandrin B (SchB), which are effective in the treatment of vascular diseases, have been known to suppress transforming growth factor β1 (TGF-β1)-mediated Smad activation and myosin light chain (MLC) phosphorylation in vascular smooth muscle cells (VSMCs). However, it is still largely unknown about the pharmacologic effects and mechanisms of SCE and SchB on TGF-β1-induced intracellular signaling pathways in vascular smooth muscle cells (VSMCs).

2017-12-20 | GSE87439 | GEO

Expression data from WT and RGS5 KO mice treated with DOCA/salt

Project description:The activation of vascular smooth muscle cells (VSMCs) during hypertension-induced arterial remodeling processes relies on a change of the gene expression program, i.e., up-regulation of genes to induce migration, proliferation and matrix degradation/synthesis. At the same time, genes controlling the quiescent, contractile VSMC phenotype are down-regulated. We used microarrays to detail the global program of gene expression underlying hypertension-induced vascular remodeling in the presence and absence of regulator of G-protein signaling 5 (RGS5) and identified distinct classes of down-regulated genes during vascular remodeling when RGS5 was not present.

2018-03-14 | GSE89073 | GEO

RBPMS promotes contractile smooth muscle splicing and alters phenotypic behaviour of human embryonic stem cell derived vascular smooth muscle cells.

Project description:Differentiated Vascular Smooth Muscle Cells (VSMCs) express a unique network of splice isoforms (smooth muscle specific alternative splicing - SM-AS) in functionally critical genes including those comprising the contractile machinery. We previously described RNA Binding Protein Multiple Splicing (RBPMS) as a potent driver of contractile, aortic tissue like SM-AS in VSMCs using rodent models. What is unknown is how RBPMS affects VSMC phenotype and behaviour. Here, we use human embryonic stem cell-derived VSMCs (hES-VSMCs) to dissect the role of RBPMS in SM-AS in human cells and determine the impact on VSMC phenotypic properties. hES-VSMCs are inherently immature and display only partially differentiated SM-AS patterns while RBPMS levels are undetectable endogenously. Hence, we used an over-expression system and found that RBPMS induces SM-AS patterns in hES-VSMCs akin to the contractile tissue VSMC splicing patterns in multiple events. We present in silico and experimental findings that support RBPMS’ splicing activity as mediated through direct binding and via functional cooperativity with splicing factor RBFOX2 on a significant subset of targets. Finally, we demonstrate that RBPMS can alter the motility and the proliferative properties of hES-VSMCs to mimic a more differentiated state. Overall, this study emphasizes a critical splicing regulatory role for RBPMS in human VSMCs and provides evidence of phenotypic modulation by RBPMS.

2024-12-19 | GSE242826 | GEO

RNA-Seq analysis Ezh2 knockdown effect on vascular smooth muscle cells

Project description:Vascular smooth muscle cells (VSMCs) phenotype switch has been thought to be critical to the development of thoracic aneurysm/dissection. To investigate the function EZH2 in the regulation of VSMCs phenotype switch, we established mouse vascular smooth muscle cells in which each target gene has been knocked down by siRNA.

2023-12-16 | GSE227177 | GEO

RNA-Seq analysis SIRT6 knockdown effect on vascular smooth muscle cells

Project description:Vascular smooth muscle cells (VSMCs) phenotype switch has been thought to be critical to the development of thoracic aneurysm/dissection. To investigate the function SIRT6 in the regulation of VSMCs phenotype switch, we established mouse vascular smooth muscle cells in which each target gene has been knocked down by siRNA.

2024-12-11 | GSE246209 | GEO

RNA-Seq analysis HDAC9 knockdown effect on vascular smooth muscle cells

Project description:Vascular smooth muscle cells (VSMCs) phenotype switch has been thought to be critical to the development of thoracic aneurysm/dissection. To investigate the function HDAC9 in the regulation of VSMCs phenotype switch, we used siRNA knockdown of HDAC9 in human aortic smooth muscle cells (HASMC)we established Human aortic smooth muscle cells (HASMCs).

2024-12-31 | GSE228573 | 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