ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008
Induction of lung emphysema is prevented by L-arginine-threonine-arginine.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 71 citations in OpenAlex.
- Targeting the proline-glycine-proline-protease feed-forward loop attenuates primary graft dysfunction after lung transplantation.Frontiers in immunology · 2026Article
- Post-Proline Cleaving Enzymes (PPCEs): Classification, Structure, Molecular Properties, and Applications.Plants (Basel, Switzerland) · 2022Review
- An in vivo model for extracellular vesicle-induced emphysema.JCI insight · 2022Article
- Highway toFrontiers in pharmacology · 2022Review
- The Counter Regulatory Axis of the Lung Renin-Angiotensin System in Severe COVID-19: Pathophysiology and Clinical Implications.Heart, lung & circulation · 2021Review
- Proline-Glycine-Proline Peptides Are Critical in the Development of Smoke-induced Emphysema.American journal of respiratory cell and molecular biology · 2019Article
- The neutrophil chemoattractant peptide proline-glycine-proline is associated with acute respiratory distress syndrome.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- An extracellular matrix fragment drives epithelial remodeling and airway hyperresponsiveness.Science translational medicine · 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
- Cigarette smoke-induced autophagy impairment accelerates lung aging, COPD-emphysema exacerbations and pathogenesis.American journal of physiology. Cell physiology · 2018Article
- Angiotensin-converting enzyme defines matrikine-regulated inflammation and fibrosis.JCI insight · 2017Article
- Feasibility and physiological relevance of designing highly potent aminopeptidase-sparing leukotriene A4 hydrolase inhibitors.Scientific reports · 2017Article
- Bioactive extracellular matrix fragments in lung health and disease.The Journal of clinical investigation · 2016Review
- The Effect of Bone Marrow Mononuclear Cells on Lung Regeneration and Apoptosis in a Simple Model of Pulmonary Emphysema.International journal of stem cells · 2016Article
- Disease phenotyping in chronic obstructive pulmonary disease: the neutrophilic endotype.Current opinion in pulmonary medicine · 2016Review
- Matrikines are key regulators in modulating the amplitude of lung inflammation in acute pulmonary infection.Nature communications · 2015Article
- Acetylation of lysine 9 on histone H3 is associated with increased pro-inflammatory cytokine release in a cigarette smoke-induced rat model through HDAC1 depression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
- The matrikine PGP as a potential biomarker in COPD.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Leukotriene A4 hydrolase: the Janus enzyme shows its ugly side in smokers.American journal of respiratory and critical care medicine · 2014Article
- Collagen degradation and neutrophilic infiltration: a vicious circle in inflammatory bowel disease.Gut · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
In patients with chronic obstructive pulmonary disease (COPD), an inflammatory process is ongoing in the lungs, with concomitant damage of the alveolar structures and loss of airway function. In this inflammatory process, extracellular matrix degradation is observed. During this lung matrix degradation, small peptide fragments consisting of proline and glycine repeats generated from collagen fibers are liberated from the matrix by matrix metalloproteinases. Chemotactic activities of these collagen-derived peptides such as N-acetyl-proline-glycine-proline (PGP) via CXCR1 and CXCR2 have been reported. We show here that PGP induces neutrophil migration in vivo, which is dose dependent. Moreover, PGP is involved in the development of emphysema-like changes in the airways. The complementary peptide, L-arginine-threonine-arginine (RTR), has been shown to bind to PGP sequences and inhibit neutrophil infiltration. We show that RTR impedes both PGP- and interleukin-8-induced chemotaxis in vitro. In vivo, RTR prevents both migration and activation of neutrophils induced by PGP. Furthermore, RTR completely inhibits PGP-induced lung emphysema, assessed by changes in alveolar enlargement and right ventricular hypertrophy. In conclusion, these data indicate that collagen breakdown products, especially PGP, are important in the pathogenesis of COPD and that PGP antagonism via RTR ameliorates lung emphysema.
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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.