ArticleThe Journal of biological chemistry2016
Proteinase 3 Is a Phosphatidylserine-binding Protein That Affects the Production and Function of Microvesicles.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- A Double-Edged Sword: Extracellular Serine Proteases as Facilitators of Infection and Mediators of Immunity.Molecules (Basel, Switzerland) · 2026Review
- Novel perspectives on extracellular vesicles in autoimmune diseases: immunogenicity, inflammation, and immune surveillance.The Journal of clinical investigation · 2026Review
- Cathepsin C-driven enhancement of neutrophil extracellular trap formation contributes to acute lung injury.iScience · 2025Article
- The promise of mesenchymal stromal/stem cells in erectile dysfunction treatment: a review of current insights and future directions.Stem cell research & therapy · 2025Review
- Interleukin-32: a Pandora's box in human immunodeficiency virus infection.Frontiers in immunology · 2025Review
- Machine learning framework develops neutrophil extracellular traps model for clinical outcome and immunotherapy response in lung adenocarcinoma.Apoptosis : an international journal on programmed cell death · 2024Article
- Innovative Diagnosis and Therapeutic Modalities: Engineered Exosomes in Autoimmune Disease.International journal of nanomedicine · 2024Review
- Review
- Phospholipid scramblase 1: a protein with multiple functions via multiple molecular interactors.Cell communication and signaling : CCS · 2022Review
- Ethanol Induces Extracellular Vesicle Secretion by Altering Lipid Metabolism through the Mitochondria-Associated ER Membranes and Sphingomyelinases.International journal of molecular sciences · 2021Article
- Recent advances in Extracellular Vesicles and their involvements in vasculitis.Free radical biology & medicine · 2021Review
- Neutrophils produce proinflammatory or anti-inflammatory extracellular vesicles depending on the environmental conditions.Journal of leukocyte biology · 2021Article
- Overcoming Chemoresistance via Extracellular Vesicle Inhibition.Frontiers in molecular biosciences · 2021Review
- Pathogenesis and pathology of anti-neutrophil cytoplasmic antibody（ANCA）-associated vasculitis.Journal of translational autoimmunity · 2021Review
- Extracellular vesicles and lupus nephritis - New insights into pathophysiology and clinical implications.Journal of autoimmunity · 2020Review
- Epstein-Barr Virus Early Protein BFRF1 Suppresses IFN-β Activity by Inhibiting the Activation of IRF3.Frontiers in immunology · 2020Article
- Potential roles of extracellular vesicles in the pathophysiology, diagnosis, and treatment of autoimmune diseases.International journal of biological sciences · 2020Review
- Role of Mac-1 integrin in generation of extracellular vesicles with antibacterial capacity from neutrophilic granulocytes.Journal of extracellular vesicles · 2020Article
- Extracellular vesicles in autoimmune vasculitis - Little dirts light the fire in blood vessels.Autoimmunity reviews · 2019Review
- Different Calcium and Src Family Kinase Signaling in Mac-1 Dependent Phagocytosis and Extracellular Vesicle Generation.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
13 authors at 10 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteinase 3 (PR3), the autoantigen in granulomatosis with polyangiitis, is expressed at the plasma membrane of resting neutrophils, and this membrane expression increases during both activation and apoptosis. Using surface plasmon resonance and protein-lipid overlay assays, this study demonstrates that PR3 is a phosphatidylserine-binding protein and this interaction is dependent on the hydrophobic patch responsible for membrane anchorage. Molecular simulations suggest that PR3 interacts with phosphatidylserine via a small number of amino acids, which engage in long lasting interactions with the lipid heads. As phosphatidylserine is a major component of microvesicles (MVs), this study also examined the consequences of this interaction on MV production and function. PR3-expressing cells produced significantly fewer MVs during both activation and apoptosis, and this reduction was dependent on the ability of PR3 to associate with the membrane as mutating the hydrophobic patch restored MV production. Functionally, activation-evoked MVs from PR3-expressing cells induced a significantly larger respiratory burst in human neutrophils compared with control MVs. Conversely, MVs generated during apoptosis inhibited the basal respiratory burst in human neutrophils, and those generated from PR3-expressing cells hampered this inhibition. Given that membrane expression of PR3 is increased in patients with granulomatosis with polyangiitis, MVs generated from neutrophils expressing membrane PR3 may potentiate oxidative damage of endothelial cells and promote the systemic inflammation observed in this disease.
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