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

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

PROVIDER: PRJNA812933 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18231034_1.fastq.gz	Fastqsanger.gz
	SRR18231034_2.fastq.gz	Fastqsanger.gz
	SRR18231035_1.fastq.gz	Fastqsanger.gz
	SRR18231035_2.fastq.gz	Fastqsanger.gz
	SRR18231036_1.fastq.gz	Fastqsanger.gz

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Vascular Regulation by Super Enhancer-Derived LINC00607 (scRNA-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 | GSE197955 | GEO

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

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 (bulk RNA-Seq)

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

| PRJNA812934 | ENA

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

Defining super-enhancer landscape in triple-negative breast cancer by multiomic profiling

Project description:Here we apply integrated epigenomic and transcriptomic profiling to uncover super-enhancer heterogeneity between breast cancer subtypes, and provide clinically relevant biological insights towards TNBC. Using CRISPR/Cas9-mediated gene editing, we identify genes that are specifically regulated by TNBC-specific super-enhancers, including FOXC1 and MET, thereby unveiling a mechanism for specific overexpression of the key oncogenes in TNBC. We also identify ANLN as a novel TNBC-specific gene regulated by super-enhancer. Our studies reveal a TNBC-specific epigenomic landscape, contributing to the dysregulated oncogene expression in breast tumorigenesis.

2021-03-04 | PXD024505 |

LSD1 inhibition disrupts super-enhancer activities in CRPC [scRNA-seq]

Project description:LSD1 inhibition disrupts super-enhancer activities in CRPC [scRNA-seq]

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Regulation of Angiotensin II Actions by Enhancers and Super-enhancers in Vascular Smooth Muscle Cells

Project description:We have profiled Ang II regulated enhancer and super-enhancers in Rat Vascular smooth muscle cells using genomewide analysis of enhancer marks H3K27ac, H3K4me1 and super-enhancer mark BRD4.

2017-12-25 | GSE95067 | GEO

Vascular Regulation by Super Enhancer-Derived LINC00607

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-20 | GSE197956 | GEO

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

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