ArticleFrontiers in immunology2022
ROS and DNA repair in spontaneous versus agonist-induced NETosis: Context matters.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Caspase-8 silences cell death-independent constitutive immune activation driven by tonic TNF-α.EMBO reports · 2026Article
- Review
- Unravelling the noncanonical extracellular DNA structures in biofilm and NETosis.Nucleic acids research · 2026Review
- Platelets in systemic lupus erythematosus: from hemostatic allies to pathogenic drivers.Frontiers in immunology · 2026Review
- Neutrophil Extracellular Traps in Systemic Lupus Erythematosus: Pathogenic Mechanisms, Crosstalk with Oxidative Stress, and Antioxidant Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- A nomogram for predicting the diagnosis of central malignant tumors based on preoperative clinical characteristics and laboratory indicators: a diagnostic study.International journal of surgery (London, England) · 2025Article
- Exploring the involvement of serine proteases in neutrophil extracellular traps: a review of mechanisms and implications.Cell death & disease · 2025Review
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Antioxidants as Modulators of NETosis: Mechanisms, Evidence, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Neutrophil Extracellular Traps (NETs) in Sterile Inflammatory Diseases.Journal of inflammation research · 2025Review
- Dapsone Alters Phenotypical and Functional Properties of Human Neutrophils In Vitro.Molecules (Basel, Switzerland) · 2024Article
- Neutrophil Extracellular Trap Formation Model Induced by Monosodium Urate and Phorbol Myristate Acetate: Involvement in MAPK Signaling Pathways.International journal of molecular sciences · 2024Article
- How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation.Biomolecules · 2024Review
- Deep learning with a small dataset predicts chromatin remodelling contribution to winter dormancy of apple axillary buds.Tree physiology · 2024Article
- Neutrophils at the Crossroads: Unraveling the Multifaceted Role in the Tumor Microenvironment.International journal of molecular sciences · 2024Review
- Subinhibitory concentrations of glabridin fromFrontiers in microbiology · 2024Article
- Mitochondrial ROS and base excision repair steps leading to DNA nick formation drive ultraviolet induced-NETosis.Frontiers in immunology · 2023Article
- A metabolic perspective of the neutrophil life cycle: new avenues in immunometabolism.Frontiers in immunology · 2023Review
- ATM and ATR, two central players of the DNA damage response, are involved in the induction of systemic acquired resistance by extracellular DNA, but not the plant wound response.Frontiers in immunology · 2023Article
- Gold Nanoparticles Encapsulated Resveratrol as an Anti-Aging Agent to Delay Cataract Development.Pharmaceuticals (Basel, Switzerland) · 2022Article
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Authors and funding
2 authors.
Funding
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Abstract
Reactive oxygen species (ROS) is essential for neutrophil extracellular trap formation (NETosis). Nevertheless, how ROS induces NETosis at baseline and during neutrophil activation is unknown. Although neutrophils carry DNA transcription, replication and repair machineries, their relevance in the short-lived mature neutrophils that carry pre-synthesized proteins has remained a mystery for decades. Our recent studies show that (i) NETosis-inducing agonists promote NETosis-specific kinase activation, genome-wide transcription that helps to decondense chromatin, and (ii) excess ROS produced by NADPH oxidase activating agonists generate genome-wide 8-oxy-guanine (8-OG), and the initial steps of DNA repair are needed to decondense chromatin in these cells. These steps require DNA repair proteins necessary for the assembly and nicking at the damaged DNA sites (poly ADP ribose polymerase PARP, apurinic endonuclease APE1 and DNA ligase), but not the enzymes that mediate the repair DNA synthesis (Proliferating cell nuclear antigen (PCNA) and DNA Polymerases). In this study, we show that (i) similar to agonist-induced NETosis, inhibition of early steps of oxidative DNA damage repair proteins suppresses spontaneous NETosis, but (ii) the inhibition of late stage repair proteins DNA polymerases and PCNA drastically promotes baseline NETosis. Hence, in the absence of excessive ROS generation and neutrophil activation, DNA repair mediated by PCNA and DNA polymerases is essential to prevent chromatin decondensation and spontaneous NETosis. These findings indicate that ROS, oxidative DNA damage, transcription and DNA repair differentially regulate spontaneous and agonist-induced NETosis. Therefore, context matters.
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