Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibition of endothelial Notch signaling attenuates inflammation

ABSTRACT: Inhibition of endothelial Notch signaling attenuates inflammation

PROVIDER: PRJNA339936 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR4340380.fastq.gz	Fastqsanger.gz
	SRR4340381.fastq.gz	Fastqsanger.gz
	SRR4340382.fastq.gz	Fastqsanger.gz
	SRR4340383.fastq.gz	Fastqsanger.gz
	SRR4340384.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Inhibition of endothelial Notch signaling attenuates inflammation [ChIP-Seq]

Project description:Vascular endothelial cells upregulate the Notch ligand Jagged1 in response to inflammatory activation. Here we show that abrogation of endothelial Notch1 signaling impairs induction of key inflammatory target genes. Accordingly, inducible endothelial-targeted knockout of the canonical Notch transcription factor RBPJ reduces inflammation in a murine model of contact hypersensitivity, while overexpression of constitutive active Notch1 has the opposite effect. We show that the proinflammatory role of Notch1 can be attributed to direct genomic priming of the inflammatory landscape involving crosstalk with NF-κB/RelA and selective activation of enhancers associated with Notch-dependent inflammatory genes. This is the first evidence that canonical Notch signaling supports endothelial activation in response to inflammatory cytokines on the chromatin level.

2018-08-29 | GSE87552 | GEO

Homo sapiens

Project description:Inhibition of endothelial Notch signaling attenuates inflammation [ChIP-Seq]

| PRJNA345175 | ENA

Inhibition of endothelial Notch signaling attenuates inflammation

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

2018-08-29 | GSE85987 | GEO

Inhibition of netosis with PAD inhibitor attenuates endotoxin shock induced systemic inflammation

Project description:Neutrophils play a pivotal role in innate immunity and participate in a range of immunological disorders. Excessive neutrophil extracellular traps formed at infection and tissue damage sites are detrimental to the local tissue and further exacerbate inflammation. Protein arginine deiminases mediate histone citrullination and NET formation thereby regulating endotoxin shock response. However, the molecular mechanisms are less known. Here we report that inhibition of netosis attenuates inflammation in a LPS induced lethal endotoxic shock model in mice. Albeit a higher number of neutrophils are accumulated in peritoneal cavity the primary inflammatory site, the level of inflammatory signals is greatly reduced after netosis inhibition with a PAD inhibitor. In lungs under endotoxic stress, gene expression analyses indicate that LPS induced a drastic increase in inflammatory gene expression. In contrast, lung tissue damage and inflammation were much reduced after PAD inhibition to reduce netosis. In summary, we found NET formation inhibition as a new avenue to manage inflammatory damages under endotoxic stress.

2022-12-01 | GSE203340 | GEO

Genome wide analysis of differential gene expression of PFKFB3 under- or overexpression upon inhibition or activation of notch signaling in endothelial cells

Project description:Analysis of gene expression profiles upon PFKFB3 under- or overexpression during inhibition or activation of notch signaling. With this experiment we aimed to identify whether alterations in PFKFB3 could influence the expression pattern of angiogenic genes in conditions that favor a tip- or stalk cell gene signature. Total RNA was collected of human umbilical vein endothelial cells either under- or overexpressing PFKFB3 and/ or have inhibited or activated notch signaling respectively. Cells were harvested 48h after manipulation of PFKFB3 and notch levels.

2013-08-01 | E-GEOD-45750 | biostudies-arrayexpress

Inhibition of netosis with PAD inhibitor attenuates endotoxin shock induced systemic inflammation

Project description:Inhibition of netosis with PAD inhibitor attenuates endotoxin shock induced systemic inflammation

| PRJNA839858 | ENA

Notch signaling rapidly regulates the expression of the small GTPase RND1 and a diverse endothelial transcriptome

Project description:Endothelial Notch signaling regulates transcription of many downstream effectors controlling sprouting, migration, proliferation, barrier formation, and other phenotypes. However, endothelial-relevant Notch targets are largely uncharacterized. Few are studied in depth, and many transient, early response Notch targets are yet to be described. We therefore determined the Notch early response transcriptional profile in several experimentally relevant in vivo and in vitro contexts: ligand-specific or EGTA-induced Notch activation in different primary endothelial cells, and gamma secretase-mediated Notch inhibition in neonatal brain endothelium in a RiboTag mouse model. The intersection of these profiles reveals a core set of early Notch-responsive targets. Among these are effectors in GPCR signaling, not previously implicated downstream of Notch signaling. We demonstrate the Rho GTPase RND1 is a direct Notch transcriptional target and required for Notch control of sprouting angiogenesis, endothelial migration and Ras activity.

2022-01-11 | GSE163568 | GEO

Heat shock protein 90 inhibition attenuates inflammation elicited by 12-O-tetradecanoylphorbol-13-acetate

Project description:Heat shock protein 90 inhibition attenuates inflammation elicited by 12-O-tetradecanoylphorbol-13-acetate

| PRJNA917298 | ENA

Loss of Vascular Endothelial Notch Signaling Induces Tertiary Lymphoid Structures in the Kidney

Project description:Tertiary lymphoid structures (TLS are lymph node-like immune cell clusters that emerge during chronic inflammation in non-lymphoid organs like the kidney, but their origin remains not well understood. Here we show, using conditional deletion strategies of the canonical Notch signaling mediator Rbpj, that loss of endothelial Notch signaling in adult mice induces the spontaneous formation of bona fide TLS in the kidney, liver and lung, based on molecular, cellular and structural criteria. These TLS form in a stereotypical manner around parenchymal arteries, while secondary lymphoid structures remained largely unchanged. This effect is mediated by endothelium of blood vessels, but not lymphatics, since a lymphatic endothelial-specific targeting strategy did not result in TLS formation, and involves loss of arterial specification and concomitant acquisition of a high endothelial cell phenotype, as shown by transcriptional analysis of kidney endothelial cells. This indicates a so far unrecognized role for vascular endothelial cells and Notch signaling in TLS initiation.

2022-02-24 | GSE193544 | GEO

Lipocalin-2 deficiency attenuates acute lung inflammation

Project description:Lipocalin-2 deficiency attenuates acute lung inflammation

| PRJNA814910 | ENA