ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Cigarette smoke-induced lung emphysema in mice is associated with prolyl endopeptidase, an enzyme involved in collagen breakdown.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 79 citations in OpenAlex.
- A Randomized, Placebo-controlled Trial of Roflumilast. Effect on Proline-Glycine-Proline and Neutrophilic Inflammation in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2015Trial
- An aberrant leukotriene A4 hydrolase-proline-glycine-proline pathway in the pathogenesis of chronic obstructive pulmonary disease.American journal of respiratory and critical care medicine · 2014Trial
- Article
- The Role of the Extracellular Matrix in the Pathogenesis and Treatment of Pulmonary Emphysema.International journal of molecular sciences · 2024Review
- Synergistic Pulmonoprotective Effect of Natural Prolyl Oligopeptidase Inhibitors in In Vitro and In Vivo Models of Acute Respiratory Distress Syndrome.International journal of molecular sciences · 2023Article
- Prolyl oligopeptidase inhibition ameliorates experimental pulmonary fibrosis both in vivo and in vitro.Respiratory research · 2023Article
- Multiscale stiffness of human emphysematous precision cut lung slices.Science advances · 2023Article
- Substrate-dependent modulation of the leukotriene AScientific reports · 2022Article
- The Counter Regulatory Axis of the Lung Renin-Angiotensin System in Severe COVID-19: Pathophysiology and Clinical Implications.Heart, lung & circulation · 2021Review
- SUL-151 Decreases Airway Neutrophilia as a Prophylactic and Therapeutic Treatment in Mice after Cigarette Smoke Exposure.International journal of molecular sciences · 2021Article
- Prenatal and Postnatal Cigarette Smoke Exposure Is Associated With Increased Risk of Exacerbated Allergic Airway Immune Responses: A Preclinical Mouse Model.Frontiers in immunology · 2021Article
- Increasing the Therapeutic Potential of Stem Cell Therapies for Critical Limb Ischemia.HSOA journal of stem cells research, development & therapy · 2020Article
- Proline-Glycine-Proline Peptides Are Critical in the Development of Smoke-induced Emphysema.American journal of respiratory cell and molecular biology · 2019Article
- Role of CXCR2 in the Ac-PGP-Induced Mobilization of Circulating Angiogenic Cells and its Therapeutic Implications.Stem cells translational medicine · 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
- 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
- The Combination Therapy of Dietary Galacto-Oligosaccharides With Budesonide Reduces Pulmonary Th2 Driving Mediators and Mast Cell Degranulation in a Murine Model of House Dust Mite Induced Asthma.Frontiers in immunology · 2018Article
- Suppression of PTPN6 exacerbates aluminum oxide nanoparticle-induced COPD-like lesions in mice through activation of STAT pathway.Particle and fibre toxicology · 2017Article
- Angiotensin-converting enzyme defines matrikine-regulated inflammation and fibrosis.JCI insight · 2017Article
- Ghrelin therapy improves lung and cardiovascular function in experimental emphysema.Respiratory research · 2017Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
There is increasing evidence that the neutrophil chemoattractant proline-glycine-proline (PGP), derived from the breakdown of the extracellular matrix, plays an important role in neutrophil recruitment to the lung. PGP formation is a multistep process involving neutrophils, metalloproteinases (MMPs), and prolyl endopeptidase (PE). This cascade of events is now investigated in the development of lung emphysema. A/J mice were whole body exposed to cigarette smoke for 20 wk. After 20 wk or 8 wk after smoking cessation, animals were killed, and bronchoalveolar lavage fluid and lung tissue were collected to analyze the neutrophilic airway inflammation, the MMP-8 and MMP-9 levels, the PE activity, and the PGP levels. Lung tissue degradation was assessed by measuring the mean linear intercept. Additionally, we investigated the effect of the peptide L-arginine-threonine-arginine (RTR), which binds to PGP sequences, on the smoke-induced neutrophil influx in the lung after 5 days of smoke exposure. Neutrophilic airway inflammation was induced by cigarette smoke exposure. MMP-8 and MMP-9 levels, PE activity, and PGP levels were elevated in the lungs of cigarette smoke-exposed mice. PE was highly expressed in epithelial and inflammatory cells (macrophages and neutrophils) in lung tissue of cigarette smoke-exposed mice. After smoking cessation, the neutrophil influx, the MMP-8 and MMP-9 levels, the PE activity, and the PGP levels were decreased or reduced to normal levels. Moreover, RTR inhibited the smoke-induced neutrophil influx in the lung after 5 days' smoke exposure. In the present murine model of cigarette smoke-induced lung emphysema, it is demonstrated for the first time that all relevant components (neutrophils, MMP-8, MMP-9, PE) involved in PGP formation from collagen are upregulated in the airways. Together with MMPs, PE may play an important role in the formation of PGP and thus in the pathophysiology of 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.