ArticleThe Journal of biological chemistry2012
Cathepsin G-regulated release of formyl peptide receptor agonists modulate neutrophil effector functions.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Single-cell and multi-omics analyses identify CAMP-associated neutrophil remodeling during radiochemotherapy in cervical cancer.Frontiers in cell and developmental biology · 2026Article
- Research Progress of Annexin A1 and Its Derived Peptides in the Diagnosis and Treatment of Circulatory Diseases.Immunity, inflammation and disease · 2025Review
- Identification and Validation of CXCL2 as a Key Gene for Childhood Obesity.Biochemical genetics · 2024Article
- Joint multi-omics discriminant analysis with consistent representation learning using PANDA.Research square · 2024Article
- Neutrophil proteases are protective against SARS-CoV-2 by degrading the spike protein and dampening virus-mediated inflammation.JCI insight · 2024Article
- The Contribution of Antimicrobial Peptides to Immune Cell Function: A Review of Recent Advances.Pharmaceutics · 2023Review
- Quantitative Proteomic Characterization of Foreign Body Response towards Silicone Breast Implants Identifies Chronological Disease-Relevant Biomarker Dynamics.Biomolecules · 2023Article
- Neutrophils and Platelets: Immune Soldiers Fighting Together in Stroke Pathophysiology.Biomedicines · 2021Review
- Article
- Evaluation of Neutrophil Activation Status According to the Phenotypes of Adult Asthma.Allergy, asthma & immunology research · 2019Article
- Ischemia-Reperfusion Injury in Sickle Cell Disease: From Basics to Therapeutics.The American journal of pathology · 2019Review
- Article
- The role of neutrophil granule proteins in neuroinflammation and Alzheimer's disease.Journal of neuroinflammation · 2018Review
- Exogenous murine antimicrobial peptide CRAMP significantly exacerbates Ovalbumin-induced airway inflammation but ameliorates oxazolone-induced intestinal colitis in BALB/c mice.Human vaccines & immunotherapeutics · 2018Article
- Cathepsin G Controls Arterial But Not Venular Myeloid Cell Recruitment.Circulation · 2016Article
- Mast cell proteases as pharmacological targets.European journal of pharmacology · 2016Review
- Genetic overexpression of Serpina3n attenuates muscular dystrophy in mice.Human molecular genetics · 2016Article
- P2X7 Receptor Regulates Internalization of Antimicrobial Peptide LL-37 by Human Macrophages That Promotes Intracellular Pathogen Clearance.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Prostaglandin E2 resistance in granulocytes from patients with aspirin-exacerbated respiratory disease.The Journal of allergy and clinical immunology · 2014Article
- Polymorphonuclear neutrophils and instability of the atherosclerotic plaque: a causative role?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neutrophil serine proteases play an important role in inflammation by modulating neutrophil effector functions. We have previously shown that neutrophils deficient in the serine proteases cathepsin G and neutrophil elastase (CG/NE neutrophils) exhibit severe defects in chemokine CXCL2 release and reactive oxygen species (ROS) production when activated on immobilized immune complex. Exogenously added active CG rescues these defects, but the mechanism remains undefined. Using a protease-based proteomic approach, we found that, in vitro, the addition of exogenous CG to immune complex-stimulated CG/NE neutrophils led to a decrease in the level of cell-associated annexin A1 (AnxA1) and cathelin-related antimicrobial peptide (CRAMP), both known inflammatory mediators. We further confirmed that, in vivo, CG was required for the extracellular release of AnxA1 and CRAMP in a subcutaneous air pouch model. In vitro, CG efficiently cleaved AnxA1, releasing the active N-terminal peptide Ac2-26, and processed CRAMP in limited fashion. Ac2-26 and CRAMP peptides enhanced the release of CXCL2 by CG/NE neutrophils in a dose-dependent manner via formyl peptide receptor (FPR) stimulation. Blockade of FPRs by an antagonist, Boc2 (t-Boc-Phe-d-Leu-Phe-d-Leu-Phe), abrogates CXCL2 release, whereas addition of FPR agonists, fMLF and F2L, relieves Boc2 inhibition. Furthermore, the addition of active CG, but not inactive CG, also relieves Boc2 inhibition. These findings suggest that CG modulates neutrophil effector functions partly by controlling the release (and proteolysis) of FPR agonists. Unexpectedly, we found that mature CRAMP, but not Ac2-26, induced ROS production through an FPR-independent pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.