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Neutrophil extracellular traps induce glomerular endothelial cell dysfunction and pyroptosis in diabetic kidney disease

ABSTRACT: Neutrophil extracellular traps induce glomerular endothelial cell dysfunction and pyroptosis in diabetic kidney disease

PROVIDER: PRJNA784943 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17074200_1.fastq.gz	Fastqsanger.gz
	SRR17074200_2.fastq.gz	Fastqsanger.gz
	SRR17074201_1.fastq.gz	Fastqsanger.gz
	SRR17074201_2.fastq.gz	Fastqsanger.gz
	SRR17074202_1.fastq.gz	Fastqsanger.gz

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Neutrophil extracellular traps induce glomerular endothelial cell dysfunction and pyroptosis in diabetic kidney disease

Project description:Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease. Neutrophil extracellular traps (NETs) are a network structure composed of loose chromatin and embedded with multiple proteins. Here, we observed increased NETs deposition in the glomeruli of DKD patients and diabetic mice (streptozotocin-induced or db/db mice). After degrading NETs with DNase I, diabetic mice exhibited attenuated glomerulopathy and glomerular endothelial cell (GEC) injury. We also observed alleviated glomerulopathy and GEC injury in peptidylarginine deiminase 4 (PAD4)-knockout mice with streptozotocin-induced diabetes. In vitro, NET-induced GEC pyroptosis was characterized by pore formation in the cell membrane, dysregulation of multiple genes involved in cell membrane function, and high expression of pyroptosis-related proteins. Strengthening the GEC surface charge by oleylamine significantly inhibited NET-induced GEC pyroptosis. These results indicate that NET-induced alterations in GEC charge are associated with GEC pyroptosis in the pathogenesis of DKD and suggest that NETs are a potential therapeutic target for DKD.

2022-09-01 | GSE189875 | GEO

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

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

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

2022-05-18 | GSE188741 | 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

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 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

Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

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

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Hydrogen gas inhibits the formation of neutrophil extracellular traps

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

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Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

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

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