ArticleEuropean journal of pharmacology2011
N-acetylated Proline-Glycine-Proline induced G-protein dependent chemotaxis of neutrophils is independent of CXCL8 release.
Article in European journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 30 citations in OpenAlex.
- Multi-omics analysis reveals neutrophil heterogeneity and key molecular drivers in sepsis-associated acute kidney injury.Frontiers in immunology · 2025Article
- Neutrophils in Tuberculosis-Associated Inflammation and Lung Pathology.Frontiers in immunology · 2020Review
- The neutrophil chemoattractant peptide proline-glycine-proline is associated with acute respiratory distress syndrome.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- The multifaceted roles of the matrikine Pro-Gly-Pro in pulmonary health and disease.European respiratory review : an official journal of the European Respiratory Society · 2018Review
- Staphylococcal Superantigen-Like Protein 1 and 5 (SSL1 & SSL5) Limit Neutrophil Chemotaxis and Migration through MMP-Inhibition.International journal of molecular sciences · 2016Article
- N-acetyl proline-glycine-proline: implications for neurological disorders.Neural regeneration research · 2016Article
- Matrix-derived inflammatory mediator N-acetyl proline-glycine-proline is neurotoxic and upregulated in brain after ischemic stroke.Journal of neuroinflammation · 2015Article
- Pharmacological antagonism of interleukin-8 receptor CXCR2 inhibits inflammatory reactivity and is neuroprotective in an animal model of Alzheimer's disease.Journal of neuroinflammation · 2015Article
- The matrikine PGP as a potential biomarker in COPD.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Matrix Metalloproteinase 9 Exerts Antiviral Activity against Respiratory Syncytial Virus.PloS one · 2015Article
- Collagen degradation and neutrophilic infiltration: a vicious circle in inflammatory bowel disease.Gut · 2014Article
- Cigarette smoke-induced collagen destruction; key to chronic neutrophilic airway inflammation?PloS one · 2013Article
- Proline-glycine-proline as a potential biomarker in chronic obstructive pulmonary disease and cystic fibrosis.Tanaffos · 2012Review
- Cigarette smoke induces β2-integrin-dependent neutrophil migration across human endothelium.Respiratory research · 2011Article
- Identification of Novel Therapeutic Targets in COPD.Tanaffos · 2011Review
- The matrikine N-α-PGP couples extracellular matrix fragmentation to endothelial permeability.Science advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Chronic inflammation in lung diseases contributes to lung tissue destruction leading to the formation of chemotactic collagen fragments such as N-acetylated Proline-Glycine-Proline (N-ac-PGP). In this study, we investigated in more detail the mechanism of action of N-ac-PGP in neutrophilic inflammation. N-ac-PGP was chemotactic for human neutrophils via pertussis toxin sensitive G protein-coupled receptors in vitro and directly activated this cell type, which led to cytosolic calcium mobilization and release of CXCL8. Furthermore, using a selective CXCR2 antagonist confirmed that N-ac-PGP-induced neutrophil chemotaxis is mediated through CXCR2 activation. To determine whether N-ac-PGP was solely responsible for the migration and activation of human neutrophils in vitro and not the released CXCL8 upon stimulation with N-ac-PGP, an antibody directed against CXCL8 was used. Performing chemotaxis and calcium influx assays in the presence of this antibody did not alter the effects of N-ac-PGP whereas effects of CXCL8 were attenuated. These experiments indicate that N-ac-PGP, in addition to the direct induction of chemotaxis, also directly activates neutrophils to release CXCL8. In vivo, this may lead in the long term to a self-maintaining situation enhanced by both N-ac-PGP and CXCL8, leading to a further increase in neutrophil infiltration and chronic inflammation.
Indexed as
Identifiers
What OpenQuestion holds
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.