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Epigenetic enhancer modifications determine the angiogenic to quiescent endothelial state transition

ABSTRACT: Epigenetic enhancer modifications determine the angiogenic to quiescent endothelial state transition

PROVIDER: PRJNA1236325 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR32699792_1.fastq.gz	Fastqsanger.gz
	SRR32699792_2.fastq.gz	Fastqsanger.gz
	SRR32699794_1.fastq.gz	Fastqsanger.gz
	SRR32699794_2.fastq.gz	Fastqsanger.gz

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Epigenetic enhancer modifications determine the angiogenic to quiescent endothelial state transition

Project description:The transcriptomic changes in endothelial cells during the state transition from the angiogenic to the quiescent phenotype are controlled by extrinsic microenvironmental factors and intrinsic epigenetic determinants. While significant progress has been made in understanding the external factors and their molecular impacts on this transition, the internal, cell-intrinsic mechanisms driving endothelial state transition remain less explored. Here, we present a detailed multiomic analysis of the epigenetic-driven state transition in angiogenic versus homeostatic lung capillary endothelial cells by mapping the histone code, accessible chromatin, and DNA methylation. Comprehensive data integration revealed selective chromatin accessibility at enhancers but not at promoters close to state-determining genes. Notably, pathological reactivation of the vasculature during tumor progression required the reestablishment of angiogenic enhancer regions to hijack developmental transcriptional programs. Enhancer reestablishment was associated with the selective expression of chromatin-modifying enzymes and the preservation of DNA hypomethylation and chromatin accessibility at former angiogenic enhancers. The data establish an enhancer-driven model of the endothelial transcriptome during angiogenic to quiescent endothelial state transition, yielding deep mechanistic insight into the dynamic epigenetic landscape governing endothelial cell function and plasticity.

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Project description:Specific Aims To identify novel transcriptional events associated with angiogenesis in VEGF and Ang-1 stimulated rat aortic rings. Our studies take advantage of the capacity of rat aortic rings to generate new vessels in collagen gels. Rat aortic rings embedded in collagen gel immediately after excision from the animal produce a self-limited angiogenic response under serum-free conditions and in the absence of exogenous stimuli. This angiogenic response can be dose-dependently promoted by vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1), which are critical regulators of the angiogenic process during embryonal development and postnatal angiogenesis. Aortic rings lose their capacity to spontaneously generate new vessels if embedded in collagen gels 10-14 days after excision. VEGF has the capacity to turn back “on” these quiescent rings producing florid angiogenesis. Conversely, Ang-1 potentiates an existing angiogenic response, but is unable to turn the quiescent system “on”. Since VEGF-mediated induction of angiogenic sprouting occurs 1-2 days of treatment, we hypothesize that this process is regulated by a unique set of “angiogenesis inducer genes” that are activated by VEGF and not by Ang-1. Identification of the proteins encoded by these genes may advance our understanding of the molecular mechanisms that regulate the earliest stages of the angiogenic cascade. Keywords: Response to growth factors

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Metabolic and transcriptomic reprogramming in the transition from a proliferative to a quiescent state is mediated by YAP-dependent and YAP-independent mechanisms.

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