Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

ABSTRACT: Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

PROVIDER: PRJNA694623 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

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

2021-01-25 | GSE165443 | GEO

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration (Neutrophils_RNA-seq)

Project description:Obesity is linked to greater cancer incidence and mortality across multiple tumor types. In breast cancer, metastasis is the leading cause of cancer-related deaths, and epidemiological studies have shown that obesity is associated with increased breast cancer metastasis to lung and liver. Using both diet-induced and genetic preclinical models of obesity, it was previously shown that obese adipose tissue systemically induces lung neutrophilia, which is associated with enhanced breast cancer metastasis to this site. Here we performed RNAseq on neutrophils isolated on the lungs from lf vs hf mice.

2021-01-25 | GSE165442 | GEO

Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration (Endothelial_Cells_RNA-seq)

2021-01-25 | GSE165441 | GEO

Project description:Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

| PRJNA667262 | ENA

Project description:Neutrophil oxidative stress mediates obesity-associated vascular inflammation and metastatic transmigration

| PRJNA667263 | ENA

Vascular Surgery Patients with Elevated Neutrophil Lymphocyte Ratios Have Downregulated Neutrophil Complement RNA Expression

Project description:Elevated NLR (neutrophil-lymphocyte ratio) in elective vascular surgery (EVS) patients is associated with increased mortality independent of perioperative surgical outcome. To understand why high NLR is associated with higher mortality, we investigated neutrophil and lymphocyte transcriptome expression in patients undergoing EVS.

2022-08-17 | GSE211190 | GEO

Gene expression profiles of Calu-3 lung epithelial cells after neutrophil transmigration

Project description:Injury to the epithelium is integral to the pathogenesis of many inflammatory lung diseases, and epithelial repair is a critical determinant of clinical outcome. However, the signaling pathways regulating such repair are incompletely understood. Herein, we used in vitro and in vivo models to define these pathways. Human neutrophils were induced to transmigrate across monolayers of human lung epithelial cells in the physiologic basolateral-to-apical direction to a gradient of fMLP. Control wells were treated with fMLP alone. Indicated wells were pretreated with an anti-CD47 blocking antibody, which exacerbates epithelial injury. This allowed study of the neutrophil contribution not only to the initial epithelial injury, but also to its repair, as manifest by restoration of transepithelial resistance (TER) and re-epithelialization of the denuded epithelium. Microarray analysis of epithelial gene expression revealed that neutrophil transmigration activated β-catenin signaling, and this was verified by real time PCR, nuclear translocation of β-catenin, and TOPFlash reporter activity. This pathway represents a potential therapeutic target to accelerate physiologic recovery in inflammatory lung diseases. Total of 20 samples: Calu-3 cells that were untreated, treated with fMLP, treated with fMLP and neutrophil transmigration, and treated with anti-CD47 antibodies, fMLP, and neutrophil transmigration; cDNA was pooled from n=3 experiments; No biological replicates

2011-08-27 | E-GEOD-31697 | biostudies-arrayexpress

Staphylococcus aureus stimulates neutrophil itaconate production that suppresses the oxidative burst

Project description:Neutrophils are critical in the host defense against Staphylococcus aureus, a major human pathogen. However, even in the setting of a robust neutrophil response, S. aureus can cause persistent infection. Here we demonstrate that S. aureus impairs neutrophil function by triggering the production of the anti-inflammatory metabolite, itaconate. The enzyme that synthesizes itaconate, Irg1, is selectively expressed in neutrophils during S. aureus pneumonia. Itaconate inhibits neutrophil glycolysis and oxidative burst, which impairs survival and bacterial killing. In a murine pneumonia model, neutrophil Irg1 expression protects critical lung cell populations from oxidative stress but compromises bacterial clearance. S. aureus is thus able to evade innate immune clearance by targeting neutrophil metabolism and inducing the production of the antiinflammatory metabolite itaconate.

2023-01-01 | GSE215195 | GEO

Vascular Surgery Patients with Elevated Neutrophil Lymphocyte Ratios Have Downregulated Neutrophil Complement RNA Expression

Project description:Vascular Surgery Patients with Elevated Neutrophil Lymphocyte Ratios Have Downregulated Neutrophil Complement RNA Expression

| PRJNA869449 | ENA

Staphylococcus aureus stimulates neutrophil itaconate production that suppresses the oxidative burst

Project description:Staphylococcus aureus stimulates neutrophil itaconate production that suppresses the oxidative burst

| PRJNA889172 | ENA