ArticleThorax2002
Expression of protease activated receptor-2 (PAR-2) in central airways of smokers and non-smokers.
Article in Thorax, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 71 citations in OpenAlex.
- Proteinase-activated receptor-2 mediates itch: a novel pathway for pruritus in human skin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Trial
- Novel risk loci encompassing genes influencing STAT3, GPCR, and oxidative stress signaling are associated with co-morbid GERD and COPD.PLoS genetics · 2025Article
- The Punicalagin Compound Mitigates Bronchial Epithelial Cell Senescence Induced by Cigarette Smoke Extract through the PAR2/mTOR Pathway.Current medicinal chemistry · 2025Article
- Airway specific deregulation of asthma-related serpins impairs tracheal architecture and oxygenation in D. melanogaster.Scientific reports · 2024Article
- Purification and characterization of a serine protease from organic dust and elucidation of its inductive effects on lung inflammatory mediators.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Protease-activated receptor 2 promotes clearance ofFrontiers in pharmacology · 2022Article
- Trypsin-Like Proteases and Their Role in Muco-Obstructive Lung Diseases.International journal of molecular sciences · 2021Review
- Astragalin Inhibits Cigarette Smoke-Induced Pulmonary Thrombosis and Alveolar Inflammation and Disrupts PAR Activation and Oxidative Stress-Responsive MAPK-Signaling.International journal of molecular sciences · 2021Article
- Airway Resistance Caused by Sphingomyelin Synthase 2 Insufficiency in Response to Cigarette Smoke.American journal of respiratory cell and molecular biology · 2020Article
- Cigarette smoke affects the onco-suppressor DAB2IP expression in bronchial epithelial cells of COPD patients.Scientific reports · 2019Article
- Protease-activated receptors (PARs): mechanisms of action and potential therapeutic modulators in PAR-driven inflammatory diseases.Thrombosis journal · 2019Review
- Cigarette smoke extract enhances neutrophil elastase-induced IL-8 production via proteinase-activated receptor-2 upregulation in human bronchial epithelial cells.Experimental & molecular medicine · 2018Article
- Proteases and oxidant stress control organic dust induction of inflammatory gene expression in lung epithelial cells.Respiratory research · 2016Article
- MD2 expression is reduced in large airways of smokers and COPD smokers.Molecular and cellular biochemistry · 2015Article
- The clinical assessment of protease-activated receptor-2 expression in inflammatory cells from peripheral blood and bronchoalveolar lavage fluid in idiopathic pulmonary fibrosis.Tuberculosis and respiratory diseases · 2013Article
- Molecular signaling and targets from itch: lessons for cough.Cough (London, England) · 2013Article
- Beta defensin-2 is reduced in central but not in distal airways of smoker COPD patients.PloS one · 2012Article
- Protease-activated receptor 2 mediates mucus secretion in the airway submucosal gland.PloS one · 2012Article
- Identification and expression patterns of members of the protease-activated receptor (PAR) gene family during zebrafish development.Developmental dynamics : an official publication of the American Association of Anatomists · 2011Article
- Protease-activated receptors and prostaglandins in inflammatory lung disease.British journal of pharmacology · 2009Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
backgroundProtease activated receptor-2 (PAR-2) is a transmembrane G protein coupled receptor preferentially activated by trypsin and tryptase. The protease activated receptors play an important role in most components of injury responses including cell proliferation, migration, matrix remodelling, and inflammation. Cigarette smoking causes an inflammatory process in the central airways, peripheral airways, lung parenchyma, and adventitia of pulmonary arteries.
methodsTo quantify the expression of PAR-2 in the central airways of smokers and non-smokers, surgical specimens obtained from 30 subjects undergoing lung resection for localised pulmonary lesions (24 with a history of cigarette smoking and six non-smoking control subjects) were examined. Central airways were immunostained with an antiserum specific for PAR-2 and PAR-2 expression was quantified using light microscopy and image analysis.
resultsPAR-2 expression was found in bronchial smooth muscle, epithelium, glands, and in the endothelium and smooth muscle of bronchial vessels. PAR-2 expression was similar in the central airways of smokers and non-smokers. When smokers were divided according to the presence of symptoms of chronic bronchitis and chronic airflow limitation, PAR-2 expression was increased in smooth muscle (median 3.8 (interquartile range 2.9-5.8) and 1.4 (1.07-3.4) respectively); glands (33.3 (18.2-43.8) and 16.2 (11.5-22.2), respectively); and bronchial vessels (54.2 (48.7-56.8) and 40.0 (36-40.4), respectively) of smokers with symptoms of chronic bronchitis with normal lung function compared with smokers with chronic airflow limitation (COPD), but the increase was statistically significant (p<0.005) only for bronchial vessels.
conclusionsPAR-2 is present in bronchial smooth muscle, glands, and bronchial vessels of both smokers and non-smokers. An increased expression of PAR-2 was found in bronchial vessels of patients with bronchitis compared with those with COPD.
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Registered trials
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