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Angioplasty induces epigenomic remodeling in injured arteries

ABSTRACT: Angioplasty induces epigenomic remodeling in injured arteries

PROVIDER: PRJNA800429 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17737105.fastq.gz	Fastqsanger.gz
	SRR17737106.fastq.gz	Fastqsanger.gz
	SRR17737107.fastq.gz	Fastqsanger.gz
	SRR17737108.fastq.gz	Fastqsanger.gz
	SRR17737109.fastq.gz	Fastqsanger.gz

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Angioplasty induces epigenomic remodeling in injured arteries

Project description:Neointimal hyperplasia (IH) is a primary etiology of stenotic vascular diseases. It is perpetuated principally by smooth muscle cell proliferation. Epigenome-scale studies concerning IH have been confined to in vitro models, and the IH-underlying epigenetic mechanisms remain poorly understood. The current study has integrated information from in vivo epigenomic mapping, conditional knockout, gene transfer and pharmacology in rodent models of IH. The data from injured (IH-prone) rat arteries revealed a surge of genomewide occupancy by H3K27me3, a gene repression mark. This was unexpected in the traditional view of prevailing post-injury gene activation rather than repression. Further analysis illustrated a shift of H3K27me3 enrichment to anti-proliferative genes, from pro-proliferative genes where gene activation mark H3K27ac instead accumulated. In accordance, H3K27ac and its reader BRD4 co-enriched at Ezh2 governing its expression. Moreover, H3K27me3 writer EZH2 positively regulated another recently identified pro-IH chromatin modulator UHRF1. Thus, results unravel injury-induced loci-specific H3K27me3 redistribution in the epigenomic landscape entailing BRD4->EZH2->UHRF1 hierarchical regulations, and may guide translation to treat IH given that these players are pharmaceutical targets.

2022-02-14 | GSE194390 | GEO

Angioplasty induces epigenomic remodeling in injured arteries.

Project description:Neointimal hyperplasia/proliferation (IH) is the primary etiology of vascular stenosis. Epigenomic studies concerning IH have been largely confined to in vitro models, and IH-underlying epigenetic mechanisms remain poorly understood. This study integrates information from in vivo epigenomic mapping, conditional knockout, gene transfer and pharmacology in rodent models of IH. The data from injured (IH-prone) rat arteries revealed a surge of genome-wide occupancy by histone-3 lysine-27 trimethylation (H3K27me3), a gene-repression mark. This was unexpected in the traditional view of prevailing post-injury gene activation rather than repression. Further analysis illustrated a shift of H3K27me3 enrichment to anti-proliferative genes, from pro-proliferative genes where gene-activation mark H3K27ac(acetylation) accumulated instead. H3K27ac and its reader BRD4 (bromodomain protein) co-enriched at Ezh2; conditional BRD4 knockout in injured mouse arteries reduced H3K27me3 and its writer EZH2, which positively regulated another pro-IH chromatin modulator UHRF1. Thus, results uncover injury-induced loci-specific H3K27me3 redistribution in the epigenomic landscape entailing BRD4→EZH2→UHRF1 hierarchical regulations. Given that these players are pharmaceutical targets, further research may help improve treatments of IH.

| S-EPMC8860099 | biostudies-literature

Transcriptional profiling from young, old, healthy, or injured rat iliac arteries.

Project description:Transcriptional profiling from young, old, healthy, or injured rat iliac arteries.

2011-10-19 | GSE29255 | GEO

mRNA-seq in the normal and injured rat carotid arteries

Project description:Our objective is to identify new miRNAs and their target mRNAs involved in arterial stenosis, especially pathological changes of smooth muscle cells. To this end, the balloon injury model was used to induce the activation of smooth muscle cells by damaging arterial endothelial cells. The balloon-injured rat carotid arteries were isolated and subjected to the RNA-Seq.

2022-10-01 | E-MTAB-11100 | biostudies-arrayexpress

Transcriptional profiling from young, old, healthy, or injured rat iliac arteries.

Project description:Transcriptional profiling from young, old, healthy, or injured rat iliac arteries. We studied the gene expression profile in a model of mechanical vascular injury in the iliac artery of aging (22 months old) and young rats (4 months old). We investigated aging-related variations in gene expression at 30 min, 3d and 7d post injury.

2011-10-18 | E-GEOD-29255 | biostudies-arrayexpress

Small RNA-seq in the normal and injured rat carotid arteries

2022-10-01 | E-MTAB-11057 | biostudies-arrayexpress

Balloon injury-induced gene expression in common carotid arteries of wistar rat

Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IM-NM-:BM-NM-1, IL-1M-NM-2) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury. Balloon injury-induced gene expression in wistar rat was measured at day 7 and day 21 after balloon injury as compared with uninjured arteries. Two independent experiments were performed at each time (uninjured, day 7 or day 21) using different wistar rats for each experiment.

2013-06-29 | E-GEOD-48279 | biostudies-arrayexpress

PTEN Deficiency Promotes Pathological Vascular Remodeling of Human Coronary Arteries

Project description:PTEN Deficiency Promotes Pathological Vascular Remodeling of Human Coronary Arteries

| PRJNA434117 | ENA

Balloon injury-induced gene expression in common carotid arteries of wistar rat

Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IκBα, IL-1β) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury.

2013-06-29 | GSE48279 | GEO

Genomewide expression profile of wire-injured carotid arteries harvested from either miR-126+/+/ApoE-/- or miR-126-/-/ApoE-/- mice during neointima development

Project description:We tried to identify mRNA targets of miR-126 involved in neointima formation in mice with an atherogenic background. Genome-wide expression profiling was carried out in wire-injured carotid arteries of miR-126+/+/ApoE-/- (control group) and miR-126-/-/ApoE-/- (target group) mice on western-type diet. RNA was isolated after 14 days following vascular injury (n=4 each group). Agilent SurePrint G3 Mouse GE Microarrays (8x60K format) were used in combination with a one-color based hybridization protocol. Signals on the microarrays were detected using the Agilent DNA Microarray Scanner. Differential gene expression was identified by applying appropriate biostatistics to the data set. GeneSpring GX11 analysis software was used to normalize and analyze the raw data Genomewide expression profile of miR-126+/+/ApoE-/- and miR-126-/-/ApoE-/- mice were measured at 14 days after vascular injury . 4 animals per group were used.

2014-02-19 | E-GEOD-34262 | biostudies-arrayexpress

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