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RNA-sequencing comparison of adipose tissue endothelial cells with Notch1 ICD overexpression

ABSTRACT: RNA-sequencing comparison of adipose tissue endothelial cells with Notch1 ICD overexpression

PROVIDER: PRJNA878482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21487500.fastq.gz	Fastqsanger.gz
	SRR21487501.fastq.gz	Fastqsanger.gz
	SRR21487502.fastq.gz	Fastqsanger.gz
	SRR21487491.fastq.gz	Fastqsanger.gz
	SRR21487492.fastq.gz	Fastqsanger.gz

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H3K27ac changes upon overexpression of the active NOTCH1 intracellular domain (N1ICD) in human adipose tissue endothelial cells.

Project description:The Notch signaling pathway regulates several differentiation and developmental processes, and is involved in the development of a multitude of diseases. Here we investigate by ChIP-Seq the effects of overexpression of the active NOTCH1 intracellular domain (N1ICD) on H3K27ac in human adipose tissue endothelial cells.

2023-06-16 | GSE195537 | GEO

RNA-sequencing comparison of adipose tissue endothelial cells with Notch1 ICD overexpression

Project description:RNA-sequencing was used to compare the transcriptome in white adipose tissue endothelial cells from humans which overexpressed N1ICD or GFP.

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H3K27ac changes upon overexpression of the active NOTCH1 intracellular domain (N1ICD) in human adipose tissue endothelial cells.

Project description:H3K27ac changes upon overexpression of the active NOTCH1 intracellular domain (N1ICD) in human adipose tissue endothelial cells.

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NOTCH1 and Endothelial Mitochondrial Metabolism

Project description:Notch signaling activation drives endothelial-to-mesenchymal transition (EndMT), which is key to heart development. Accumulating evidence indicates that endothelial cell metabolism reprogramming regulates endothelial function independent of canonical cell signaling. Herein, we investigated whether and how Notch signaling and metabolism reprogramming crosstalk in the EndMT process. We found Notch1 intracellular domain (NICD1) was localized within the mitochondria of endothelial cells and interacted with the PDH E1 subunit beta, influencing the phosphorylation of the PDH E1 subunit alpha, thereby activating PDH and enhancing mitochondrial metabolism.

2025-01-18 | PXD054146 | Pride

Notch1 dose modulates endothelial gene expression

Project description:Purpose: To use RNA-Seq analysis of endothelial cell in various Notch1 alllels in order to determine transcrptional differencesas a consequence of Notch dose. Methods: Using a FACS sorting we generated high-throughput RNA-SEQ data of endothelials in various Notch1 alleles during development Results: Notch1 dose can alter gene expression in a subset of endothelial genes RNA-Seq was performed on endothelial cells isolated at e9.5 from embryos with various Notch1 alleles including N1+/+, N1+/-, N1+/vg, N112/vg, N112/-

2015-08-04 | E-GEOD-69276 | biostudies-arrayexpress

N1ICD overexpression effect on white adipose tissue

Project description:Analysis of inguinal white adipose tissue (WAT) isolated from wildtype (WT) and Notch1 overexpression mice (Ad/NICD). Results provide insight into molecular mechanisms underlying lipodystrophy of Ad/NICD mice

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Notch1 dose modulates endothelial gene expression

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Gene expression data from endothelial cells isolated from DNFB-treated ears of mice with inducible endothelial-specific overexpression of constitutively active Notch1 intracellular domain

Project description:Notch1 is a key regulator of endothelial cell behaviour. This experiment was designed to identify genes regulated by Notch1 signaling in inflammatory activated mouse endothelial cells.

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Endothelial NOTCH1 is suppressed by circulating lipids and antagonizes inflammation during atherosclerosis

Project description:While much progress has been made in identifying the mechanisms that trigger endothelial activation and inflammatory cell recruitment during atherosclerosis, less is known about the intrinsic pathways that counteract these events. Here we identified NOTCH1 as an antagonist of endothelial cell activation. NOTCH1 was constitutively expressed by adult arterial endothelium, but levels were significantly reduced by high fat diet. Furthermore, treatment of human aortic endothelial cells (HAEC) with inflammatory lipids (Ox-PAPC) and pro-inflammatory cytokines (TNFalpha and IL1beta) decreased Notch1 expression and signaling in vitro through a mechanism that requires STAT3 activation. Reduction of NOTCH1 in HAEC by siRNA, in the absence of inflammatory lipids or cytokines, increased inflammatory molecules and binding of monocytes. Conversely, some of the effects mediated by Ox-PAPC were reversed by increased NOTCH1 signaling; suggesting a link between lipid-mediated inflammation and Notch1. Interestingly, reduction of NOTCH1 by Ox-PAPC in HAEC was associated with a genetic variant previously correlated to HDL in a human GWAS. Finally endothelial Notch1 heterozygous mice showed higher diet-induced atherosclerosis. Based on these findings, we propose that reduction of endothelial NOTCH1 is a predisposing factor in the onset of vascular inflammation and initiation of atherosclerosis. Transcript profile from Human Aortic Endothelial Cells (HAEC) transfected with siRNA targeting NOTCH1 (n=3) or treated with Ox-PAPC (Oxidized 1-Palmitoyl-2-Arachidonoyl-sn-glycero-3-PhosphoCholine) for 6 hours (n=3) were compared to control HAEC (transfected with control siRNA and control media; n=3).

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Expression data from a mouse small cell lung cancer (SCLC) cell line, KP1, transfected with Notch-ICD

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