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Homo sapiens

ABSTRACT: Genome-wide maps of H3K27ac, PPARβ/δ and Pol II localization in HUVECs

PROVIDER: PRJNA216152 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR955830.fastq.gz	Fastqsanger.gz
	SRR955831.fastq.gz	Fastqsanger.gz
	SRR955832.fastq.gz	Fastqsanger.gz
	SRR955833.fastq.gz	Fastqsanger.gz
	SRR955834.fastq.gz	Fastqsanger.gz

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Genome-wide maps of H3K27ac, PPARβ/δ and Pol II localization in HUVECs

Project description:H3K27Ac is one of the expressed enhancer markers, PPARβ/δ is a transcription factor and Pol II (RNA polymerase II) is an enzyme which catalyzes the transcription of DNA to synthesize precursors of mRNA and most snRNA and microRNA. These genomic localization in endothelial cells is unknown in endothelial cells. This time, we established a new antibody for H3K27ac, PPARβ/δ and Pol II and performed ChIP-seq to identify H3K27ac, PPARβ/δ and Pol II binding site in whole genome manner under PPARβ/δ agonist and/or hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with PPARβ/δ agonist (GW501516 100nM) and/or hypoxia (1%O2) for 24hours, then H3K27ac, PPARβ/δ and Pol II binding regions were identified. Normoxia and DMSO was used as a control condition. HUVECs were used within the first 6 passages.

2014-03-06 | E-GEOD-50144 | biostudies-arrayexpress

Genome-wide maps of H3K27ac, PPARβ/δ and Pol II localization in HUVECs

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Project description:Genome-wide maps of H3K27ac localization in HUVECs

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Expression data of HUVEC cells after PPARβ/δ agonist and/or hypoxia treatment

Project description:Recently the role of PPARβ/δ in angiogenesis has been revealed, and we hypothesized that the crosstalk between hypoxia and PPARβ/δ on endothelial cells may exsist. To elucidate the interaction between two signalings, we report the comprehensive change of transcripts induced by PPARβ/δ agonist (GW501516) and/or hypoxia. We used microarray analysis of HUVECs treated with PPARβ/δ agonist (GW501516) and/or hypoxia (1% O2) for 24-hours, and we identified a group of consistently up- or down-regulated genes. HUVECs were used within the first 6 passages. HUVECs were treated with PPARβ/δ agonist (GW501516) at a concentration of 100 nM and/or hypoxia (1% O2) for 24-hours. Same concentration of DMSO was used as a control sample, and as to the oxgen, normoxia was used as a control condition.

2014-03-06 | E-GEOD-50378 | biostudies-arrayexpress

Expression data of HUVEC cells after PPARβ/δ agonist and/or hypoxia treatment

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Project description:Genome-wide maps of RNA Polymerase II and p65 localization in HUVECs stimulated with TNF alpha

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Genome-wide map of 4 histone modifications and PolII in iPSC-derived human cardiomyocytes

Project description:We generated maps of H3K4me1, H3K27ac (enhancers), H3K4me3, Pol II (promoters) and H3K27me3 (repressed chromatin) in the genome of human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by ChIP-seq of H3K27ac, H34me1, H327me3, H3K4me3 and PolII

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Vascular PPARb/d Promotes Tumor Angiogenesis and Progression

Project description:PPARβ/δ has been suggested to be involved in the regulation of the angiogenic switch in tumor progression. However, until now it is not clear to what extent the expression of PPARβ/δ in tumor endothelium influences tumor progression and metastasis formation. We addressed this question using transgenic mice with an inducible conditional vascular-specific overexpression of PPARβ/δ. Following specific over-expression of PPARβ/δ in endothelial cells, we induced syngenic tumors. We observed an enhanced tumor growth, a higher vessel density, and enhanced metastasis formation in the tumors of animals with vessel-specific overexpression of PPARβ/δ. In order to identify molecular downstream targets of PPARβ/δ in the tumor endothelium, we sorted endothelial cells from the tumors and performed RNA sequencing.We show here that PPARβ/δ activation, regardless of its action on different cancer cell types, leads to a higher tumor vascularization which favors tumor growth and metastasis formation.

2019-12-12 | GSE140513 | GEO

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