Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Vascular Regulation by Super Enhancer-Derived LINC00607 (scRNA-Seq)

ABSTRACT: Vascular endothelial cells play a pivotal role in whole body homeostasis. Recent advances have revealed enhancer-associated long non-coding RNAs as essential regulators in endothelial function. We investigated LINC00607, a super enhancer-derived in human arteries with an emphasis on endothelial cells. Using a series of RNA-sequencing, we characterized the transcriptomes regulated by LINC00607 in endothelial cells and vascular smooth muscle cells, and in basal and diabetic conditions in endothelial cells. Furthermore, using scRNA-seq, we demonstrated that modified antisense oligonucleotide inhibitor of LINC00607 can reverse key dysfunctional changes induced by high glucose and TNF-alpha in endothelial cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE197955 | GEO | 2022/07/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Vascular Regulation by Super Enhancer-Derived LINC00607 (bulk RNA-Seq)

Project description:Vascular endothelial cells play a pivotal role in whole body homeostasis. Recent advances have revealed enhancer-associated long non-coding RNAs as essential regulators in endothelial function. We investigated LINC00607, a super enhancer-derived in human arteries with an emphasis on endothelial cells. Using a series of RNA-sequencing, we characterized the transcriptomes regulated by LINC00607 in endothelial cells and vascular smooth muscle cells, and in basal and diabetic conditions in endothelial cells. Furthermore, using scRNA-seq, we demonstrated that modified antisense oligonucleotide inhibitor of LINC00607 can reverse key dysfunctional changes induced by high glucose and TNF-alpha in endothelial cells.

2022-07-20 | GSE197954 | GEO

Vascular Regulation by Super Enhancer-Derived LINC00607

Project description:Vascular Regulation by Super Enhancer-Derived LINC00607

| PRJNA812931 | ENA

Vascular Regulation by Super Enhancer-Derived LINC00607 (scRNA-Seq)

Project description:Vascular Regulation by Super Enhancer-Derived LINC00607 (scRNA-Seq)

| PRJNA812933 | ENA

LINC00607 is essential to maintain the endothelial phenotype through SWI/SNF chromatin remodeler BRG1

Project description:Long non-coding RNAs (lncRNAs) are regulatory RNAs, which by altering gene expression impact on the cellular phenotype and cardiovascular disease development. The pool of endothelial lncRNAs and their vascular function is largely undefined. Deep-endothelial RNA-Seq and FANTOM5 CAGE analysis revealed LINC00607 as a specifically enriched and highly expressed lncRNA in human endothelial cells. LINC00607 was induced in response to hypoxia, arteriosclerosis regression in non-human primates and also in response to propranolol used to induce regression of human arteriovenous malformations. siRNA Knockdown or CRISPR/Cas9 knockout of LINC00607 attenuated VEGF-A-induced angiogenic sprouting. LINC00607 knockout HUVEC also integrated less into newly formed vascular networks in an in vivo assay in SCID mice. Overexpression of LINC00607 in CRISPR knockout cells restored the normal function. RNA- and ATAC-Seq of the LINC00607 knockout revealed changes in transcription of endothelial gene sets particularly linked to the endothelial phenotype. This was most likely the consequence of a reduced chromatin accessibility of the ERG binding motif. Mechanistically, LINC00607 interacts with the SWI/SNF chromatin remodeling protein BRG1. CRISPR/Cas9-mediated knockout of BRG1 in HUVEC followed by CUT&RUN revealed that BRG1 is required to secure a stable chromatin state, mainly on ERG-binding sites. In conclusion, LINC00607 is a highly expressed endothelial-specific lncRNA important for efficient endothelial gene transcription through sustaining ERG target gene transcription by interaction with the chromatin remodeler BRG1.

2023-01-09 | GSE201824 | GEO

Vascular Regulation by Super Enhancer-Derived LINC00607 (bulk RNA-Seq)

Project description:Vascular Regulation by Super Enhancer-Derived LINC00607 (bulk RNA-Seq)

| PRJNA812934 | ENA

Transcriptomic changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [RNA-seq]

Project description:Long non-coding RNAs (lncRNAs) are molecular switches in cellular differentiation, movement and in the reprogramming of cell states by altering gene expression patterns. However, in endothelial cells their role is not well understood. LINC00607 is an endothelial-enriched lncRNA. In order to uncover the functional relevance of LINC00607, an endothelial lentiCRISPR/Cas9-mediated knock-out was created and subjected to RNA- and ATAC-Seq, which revealed that LINC00607 is important for many pathways, among them VEGF- and TGF-beta-signalling.

2023-01-09 | GSE199877 | GEO

Chromatin accessibility changes after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC [ATAC-seq]

2023-01-09 | GSE199876 | GEO

Vascular Regulation by Super Enhancer-Derived LINC00607.

Project description:Vascular endothelial cells (ECs) play a pivotal role in whole body homeostasis. Recent advances have revealed enhancer-associated long non-coding RNAs (lncRNAs) as essential regulators in EC function. We investigated LINC00607, a super enhancer-derived lncRNA (SE-lncRNA) in human arteries with an emphasis on ECs. Based on public databases and our single cell RNA-sequencing (scRNA-seq) data from human arteries collected from healthy and diabetic donors, we found that LINC00607 is abundantly expressed in the arteries and its level is increased in diabetic humans. Using RNA-sequencing, we characterized the transcriptomes regulated by LINC00607 in ECs and vascular smooth muscle cells (VSMCs) and in basal and diabetic conditions in ECs. Furthermore, through transcriptomic and promoter analysis, we identified c-Myc as an upstream transcription factor of LINC00607. Finally, using scRNA-seq, we demonstrated that modified antisense oligonucleotide inhibitor of LINC00607 can reverse dysfunctional changes induced by high glucose and TNFα in ECs. Collectively, our study demonstrates a multi-pronged approach to characterize LINC00607 in vascular cells and its gene regulatory networks in ECs and VSMCs. Our findings provide new insights into the regulation and function of SE-derived lncRNAs in both vascular homeostasis and dysfunction in a cell-type and context-dependent manner, which could have a significant impact on our understanding of epigenetic regulation implicated in cardiovascular health and diseases like diabetes.

| S-EPMC9274098 | biostudies-literature

Comparison of young and aged F344 rat coronary artery

Project description:Previous studies showed that aging in coronary arteries is associated with pro-inflammatory phenotypic changes and decreased NO bioavailability, which, we hypothesized, promotes vascular disease by inducing endothelial apoptosis. To test this hypothesis we characterized pro-apoptotic alterations in the phenotype of coronary arteries of aged (26 month old) and young (3 month old) F344 rats. DNA fragmentation analysis and TUNEL assay showed that in aged vessels there was a ~4 fold increase in the number of apoptotic endothelial cells. Analysis of the expression of apoptosis-related genes (real-time PCR) showed that in aged coronary arteries there was an increased expression of TNFa, TNFb, caspase 9 and an increased presence of cleaved caspase 3 and caspase 9 (Western blotting), whereas expression of TNFR1 and that of TRADD, Bcl-2, Bcl-X(L), Bid, Bax, caspase 8 and caspase 3 were unchanged. Vascular expression and activity of TNFa convertase enzyme were preserved in aging. We propose that aging-induced up-regulation of TNFa and decreased bioavailability of NO promote endothelial apoptosis in coronary arteries that may lead to the development of endothelial dysfunction and ischemic heart disease in the elderly.

2010-06-05 | E-GEOD-619 | biostudies-arrayexpress

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers [Affymetrix]

Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. Gene expression analysis of human endothelial cells in resting state, treatment with TNFalpha or TNFalpha with the BET bromodomain inhibitor JQ1

2014-09-29 | E-GEOD-53999 | 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