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ATAC-seq and RNA-seq after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC

ABSTRACT: ATAC-seq and RNA-seq after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC

PROVIDER: PRJNA821874 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18560344_1.fastq.gz	Fastqsanger.gz
	SRR18560344_2.fastq.gz	Fastqsanger.gz
	SRR18560345_1.fastq.gz	Fastqsanger.gz
	SRR18560345_2.fastq.gz	Fastqsanger.gz
	SRR18560346_1.fastq.gz	Fastqsanger.gz

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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]

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

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

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

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

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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

ATAC-seq and RNA-seq after CRISPR/Cas9-mediated knock-out of lncRNA LINC00607 in HUVEC

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

2023-01-09 | GSE199878 | GEO

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.

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

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RNA-Seq of HUVEC

Project description:RNA-Seq of HUVEC

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