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Piezo1 induces neutrophil extracellular traps formation directing M1 macrophage differentiation

ABSTRACT: Piezo1 induces neutrophil extracellular traps formation directing M1 macrophage differentiation

PROVIDER: PRJNA909220 | ENA |

REPOSITORIES: ENA

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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

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

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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.

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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.

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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.

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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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Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

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Hydrogen gas inhibits the formation of neutrophil extracellular traps

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RNA-seq of wildtype and PIEZO1 knockout mice livers to investigate lipid and glucose regulation by the endothelial force sensor PIEZO1

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