Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MRNA, ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

ABSTRACT: ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

ORGANISM(S): Homo sapiens

PROVIDER: GSE188741 | GEO | 2022/05/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

mRNA, ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

Project description:mRNA, ncRNA-seq and miRNA-seq of AGS cellline and AGS cellline with neutrophil extracellular traps

| PRJNA780026 | ENA

Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.

Project description:This SuperSeries is composed of the following subset Series: GSE32542: Murine serum reactivity to common autoantigens in response to immunization with neutrophil extracellular traps GSE32543: Human and murine serum reactivity to specific histone posttranslational modifications in neutrophil extracellular traps Refer to individual Series

2012-01-26 | E-GEOD-32544 | biostudies-arrayexpress

Piezo1 induces neutrophil extracellular traps formation directing M1 macrophage differentiation

Project description:To research the neutrophil extracellular traps in the regulation of macrophages differentiation, we performed gene expression profiling analysis using data obtained from RNA-seq of mice and control with virus infection.

2024-07-10 | GSE220198 | GEO

Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

Project description:Cerebral Cavernous Malformation (CCM) is a brain vascular disease with various neurological symptoms. In this study, we describe the inflammatory profile in CCM and show for the first time the formation of neutrophil extracellular traps (NETs) in rodents and humans with CCM. Through RNA-seq analysis of cerebellum endothelial cells from wild-type mice and mice with anendothelial cell-specific ablation of the Ccm3 gene (Ccm3iECKO), we show that endothelial cells from Ccm3iECKO mice have anincreased expression of inflammation-related genes.

2023-10-31 | GSE246373 | GEO

Neutrophil extracellular traps mediate articular cartilage damage and enhance the immunogenicity of cartilage components in rheumatoid arthritis

Project description:This study invesigates the effects of neutrophil extracellular traps (NETs) on articular cartilage degredation and resulting autoimmune responses in rheumatoid arthritis.

2020-08-10 | GSE150466 | GEO

Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

Project description:Neutrophil recruitment and activation are hallmarks of the prevalent inflammatory disease, periodontitis. However, the mechanisms by which neutrophils contribute to in inflammatory bone destruction remain unclear. Herein, we document that neutrophil extracellular traps (NETs) have a direct role in mediating inflammatory pathology. In an established animal model of periodontitis, we demonstrate that genetic or pharmacologic inhibition of NETs formation, or removal of NETs by DNase-Ⅰ, alleviates inflammatory bone loss in vivo. Investigating the mechanisms by which NETs drive periodontal inflammation, we find that extracellular histones have a direct role in disease progression. Consistent with findings in animal models, histones bearing classic NET-associated post-translational modifications are correlated with disease severity and are significantly elevated in local lesions and systemic circulation of patients with periodontitis. Our work reveals NETs-associated components as pathogenic mediators, potential biomarkers, and therapeutic targets for periodontitis.

2023-05-23 | GSE228021 | GEO

Hydrogen gas inhibits the formation of neutrophil extracellular traps

Project description:Hydrogen gas inhibits the formation of neutrophil extracellular traps

| PRJNA741395 | ENA

Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

Project description:Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

| PRJNA947673 | ENA

Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

Project description:Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

| PRJNA1032618 | ENA

Hydrogen gas inhibits the formation of neutrophil extracellular traps

Project description:Neutrophil extracellular traps (NETs) contribute to inflammatory pathogenesis, especially in infectious and cardiovascular diseases. H2 gas acts as an antioxidant and has been clinically and experimentally proven to ameliorate inflammation. Therefore, we investigated whether H2 gas could inhibit NET formation associated with excessive neutrophil activation. Phorbol-12-myristate-13-acetate (PMA)-stimulated human neutrophils exposed to H2 exhibited reduced citrullination of histones, membrane disruption by chromatin complexes, and release of NET components over controls. Mechanistically, H2 suppressed the phosphorylation of Ser-139 residue in H2AX, a marker of DNA damage, thereby reducing the expression of CXC-chemokine receptor 4 (CXCR4) in PMA-stimulated neutrophils. Along with the upregulation of CXCR4, the intracellular content of myeloperoxidase (MPO) and the production of MPO-derived hypochlorous acid (HOCl) was increased; however, these effects were markedly suppressed in H2-exposed cultures. Thus, H2 neutralized HOCl produced by the oxidative burst, inhibited DNA damage, and subsequently inhibited NET formation. We further confirmed that inhalation of H2 inhibited the formation and release of NET components in the blood and bronchoalveolar lavage of a lipopolysaccharide-induced sepsis model in mice and aged minipigs. Therefore, H2 therapy has the potential to be a new therapeutic agent for inflammatory diseases involving NETs associated with excessive neutrophil activation.

2022-02-23 | GSE178883 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data