ArticlePloS one2013
Reactivation of desensitized formyl peptide receptors by platelet activating factor: a novel receptor cross talk mechanism regulating neutrophil superoxide anion production.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 54 citations in OpenAlex.
- Platelet-Activating Factor Promotes Neutrophil Activation and Platelet-Neutrophil Complex Formation.Scandinavian journal of immunology · 2025Article
- TheFrontiers in immunology · 2025Review
- The allosterically modulated FFAR2 is transactivated by signals generated by other neutrophil GPCRs.PloS one · 2023Article
- Immune Cell Plasticity in Inflammation: Insights into Description and Regulation of Immune Cell Phenotypes.Cells · 2022Review
- The Antimicrobial Activity of Peripheral Blood Neutrophils Is Altered in Patients with Primary Ciliary Dyskinesia.International journal of molecular sciences · 2021Article
- Functional selective FPR1 signaling in favor of an activation of the neutrophil superoxide generating NOX2 complex.Journal of leukocyte biology · 2021Article
- The Two Formyl Peptide Receptors Differently Regulate GPR84-Mediated Neutrophil NADPH Oxidase Activity.Journal of innate immunity · 2021Article
- Data showing effects of a PI3K-δ inhibitor on neutrophil superoxide production during FPR2 activation and reactivation.Data in brief · 2020Article
- Neutrophil chemoattractant receptors in health and disease: double-edged swords.Cellular & molecular immunology · 2020Review
- Neutrophil Signaling That Challenges Dogmata of G Protein-Coupled Receptor Regulated Functions.ACS pharmacology & translational science · 2020Review
- Update on Neutrophil Function in Severe Inflammation.Frontiers in immunology · 2018Review
- Formyl Met-Leu-Phe-Stimulated FPR1 Phosphorylation in Plate-Adherent Human Neutrophils: Enhanced Proteolysis but Lack of Inhibition by Platelet-Activating Factor.Journal of immunology research · 2018Article
- The Lipidated Peptidomimetic Lau-((S)-Aoc)-(Lys-βNphe)6-NH2 Is a Novel Formyl Peptide Receptor 2 Agonist That Activates Both Human and Mouse Neutrophil NADPH Oxidase.The Journal of biological chemistry · 2016Article
- The role of neutrophils in immune dysfunction during severe inflammation.Critical care (London, England) · 2016Review
- Gelsolin and Progression of Aortic Arch Calcification in Chronic Hemodialysis Patients.International journal of medical sciences · 2016Article
- Enemy attraction: bacterial agonists for leukocyte chemotaxis receptors.Nature reviews. Microbiology · 2015Review
- Human neutrophil formyl peptide receptor phosphorylation and the mucosal inflammatory response.Journal of leukocyte biology · 2015Article
- Platelet Activating Factor Enhances Synaptic Vesicle Exocytosis Via PKC, Elevated Intracellular Calcium, and Modulation of Synapsin 1 Dynamics and Phosphorylation.Frontiers in cellular neuroscience · 2015Article
- CFP-10 from Mycobacterium tuberculosis selectively activates human neutrophils through a pertussis toxin-sensitive chemotactic receptor.Infection and immunity · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils express different chemoattractant receptors of importance for guiding the cells from the blood stream to sites of inflammation. These receptors communicate with one another, a cross talk manifested as hierarchical, heterologous receptor desensitization. We describe a new receptor cross talk mechanism, by which desensitized formyl peptide receptors (FPRdes) can be reactivated. FPR desensitization is induced through binding of specific FPR agonists and is reached after a short period of active signaling. The mechanism that transfers the receptor to a non-signaling desensitized state is not known, and a signaling pathway has so far not been described, that transfers FPRdes back to an active signaling state. The reactivation signal was generated by PAF stimulation of its receptor (PAFR) and the cross talk was uni-directional. LatrunculinA, an inhibitor of actin polymerization, induced a similar reactivation of FPRdes as PAF while the phosphatase inhibitor CalyculinA inhibited reactivation, suggesting a role for the actin cytoskeleton in receptor desensitization and reactivation. The activated PAFR could, however, reactivate FPRdes also when the cytoskeleton was disrupted prior to activation. The receptor cross talk model presented prophesies that the contact on the inner leaflet of the plasma membrane that blocks signaling between the G-protein and the FPR is not a point of no return; the receptor cross-talk from the PAFRs to the FPRdes initiates an actin-independent signaling pathway that turns desensitized receptors back to a signaling state. This represents a novel mechanism for amplification of neutrophil production of reactive oxygen species.
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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.