Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Estrogen-induced NETs promote aseptic inflammation via NKCC1

ABSTRACT: Estrogen-induced NETs promote aseptic inflammation via NKCC1

PROVIDER: PRJNA927007 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Estrogen-induced NETs promote aseptic inflammation via NKCC1 [human]

Project description:Estrogen-induced NETs promote aseptic inflammation via NKCC1 [human]

| PRJNA927014 | ENA

Estrogen-induced NETs promote aseptic inflammation via NKCC1 [human]

Project description:Although the formation of neutrophil extracellular traps (NETs) is caused by inflammation-related factors, it remains unclear whether endogenous hormones promote NET formation. Here, we investigate NET formation between infection-driven inflammatory endometrium and estrogen-induced hyperplastic endometrium by single-cell multiomics analysis. We identified a unique neutrophil subpopulation (CD24high neutrophil) involved in estrogen-driven NET formation. Estrogen-induced NETs mainly form due to the imbalance of histone caused by estrogen receptors. Inhibition of NETs significantly ameliorated endometrial hyperplasia (EH) in a murine model. Mechanistically, NETs promote cell proliferation by binding to NKCC1 on epithelial cells. Aspirin was screened to inhibit NET formation and alleviated EH in cynomolgus monkey. This study provides a novel nonhormone replacement therapy to treat patients with estrogen abnormalities by targeting NETs.

2025-01-29 | GSE223639 | GEO

Neutrophil Extracellular Traps (NETs) promote macrophage inflammation and impair atherosclerosis resolution in mice with diabetes

Project description:Neutrophil extracellular traps (NETs) promote inflammation and atherosclerosis progression. In diabetes they are increased and impair wound healing, during which inflammation normally resolves. Atherosclerosis regression, a process resembling wound healing, is also impaired in diabetes. Thus, we hypothesized that NETs impede atherosclerosis regression in diabetes through unresolved inflammation. Objective: To investigate in diabetes the effect of NETs on plaque macrophage inflammation and whether NETs reduction improves atherosclerosis regression. Findings: Transcriptomic profiling of plaque macrophages from NET positive and negative areas in Ldlr-/- mice revealed inflammasome and glycolysis pathway upregulation, indicating a pro-inflammatory phenotype. During atherosclerosis regression in non-diabetic mice, plaque NET content decreased. In contrast, in diabetic mouse plaques NETs were enriched and persisted after lipid-lowering. DNase1 treatment (to degrade NETs) of diabetic mice reduced plaque NETs and macrophage inflammation and improved atherosclerosis regression after lipid-lowering. Conclusions: NETs decline during atherosclerosis regression in non-diabetic mice, but persist in diabetes and impair regression by exacerbating macrophage inflammation. DNase1 reduced diabetic plaque NETs and macrophage inflammation, and restored atherosclerosis resolution after lipid-lowering, despite ongoing hyperglycemia. Given that humans with diabetes also exhibit impaired atherosclerosis resolution with lipid-lowering, these data suggest that NETs contribute to the increased CVD risk in this population.

2020-05-12 | GSE145200 | GEO

Neutrophil Extracellular Traps (NETs) promote macrophage inflammation and impair atherosclerosis resolution in mice with diabetes

Project description:Neutrophil Extracellular Traps (NETs) promote macrophage inflammation and impair atherosclerosis resolution in mice with diabetes

| PRJNA606287 | ENA

Estrogen-induced NETs promote aseptic inflammation via NKCC1

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

2025-01-31 | GSE223643 | GEO

NETOME: The Molecular Characterization of Neutrophil Extracellular Traps (NETs)

Project description:Neutrophils are necessary in mamalian’s life and are the most abundant type of white blood cells in humans with biological roles relevant to inflammation and the entire host response. The release of neutrophil extracellular DNA in innate immune cells provides specific response to bacteria and fungi. Neutrophil Extracellular Traps (NETs) act as antimicrobial agents and activators of immune response through release of the nuclear content into the extracellular space. Although great strides have been made in dissecting cellular and molecular pathways that control NET formation, the exact molecular composition of released NETs has not been elucidated. Here, we open the field of NETOMIC studies through isolation of NETs in combination with shotgun genomics and proteomics. This study reveals the molecular composition of NETs and specific expression regions of NETs induced in a sterile inflammation system. The existence of an in vitro NET isolation model allowed for an unprecedented amount of replicability. Additional studies are needed to verify the specificity of these sequences in the context of human health and disease upon diverse neutrophil microbial challenges.

2022-10-25 | PXD016143 | Pride

Kuiyangling inhibits inflammation by reducing intestinal NETs in mice with ulcerative colitis

Project description:Kuiyangling inhibits inflammation by reducing intestinal NETs in mice with ulcerative colitis

| PRJNA935943 | ENA

MAFG-driven astrocytes promote CNS inflammation

Project description:MAFG-driven astrocytes promote CNS inflammation

| PRJNA534022 | ENA

The effect of neutrophil extracellular trap (NETs) on BMDMs

Project description:To investigate the altered gene expression levels in BMDMs treated with or without NETs. Each group had a biological repeat (n=3). Results provide insight into the effect of NETs on BMDMs.

2024-11-27 | GSE268729 | GEO

RNA Sequencing reveals transcriptome profiling of HUVECs in response to NETs ± defibrotide

Project description:We reported the application of RNA sequecing to broadly understand the pathways associated with HUVECs exposed to vehicle, NETs, or NETs + defibrotide. We identified 440 differentially expressed genes (300 upregulated) in HUVECs upon NET stimulation as compared with vehicle. Conversely, there were 229 differentially expressed genes (192 downregulated) when the NETs + defibrotide group was compared to NETs alone.

2021-10-13 | GSE179828 | 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