ArticleThorax2012
uPAR regulates bronchial epithelial repair in vitro and is elevated in asthmatic epithelium.
Article in Thorax, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- uPAR deficiency triggers TGFβ1-mediated fibrotic remodeling in a cardiac perivascular-like microenvironment.Stem cell research & therapy · 2026Article
- Impact of obesity on airway remodeling in asthma: pathophysiological insights and clinical implications.Frontiers in allergy · 2024Review
- Elevated PLAUR is observed in the airway epithelium of asthma patients and blocking improves barrier integrity.Clinical and translational allergy · 2023Article
- PLAUR splicing pattern in hereditary angioedema patients' monocytes and macrophages.Molecular biology reports · 2023Article
- Expression of CCR8 and CCX-CKR on Basophils in Chronic Urticaria Is Amplified by IgE-Mediated Activation.Biomedicines · 2023Article
- Article
- Network-based integrated analysis for toxic effects of high-concentration formaldehyde inhalation exposure through the toxicogenomic approach.Scientific reports · 2022Article
- suPAR to Risk-Stratify Patients With Malaria.Frontiers in immunology · 2022Review
- Relationship Between Soluble Urokinase Plasminogen Activator Receptor (suPAR) and Disease Outcome in Adult-Onset Asthma.Journal of asthma and allergy · 2022Article
- Mast Cell Proteases Tryptase and Chymase Induce Migratory and Morphological Alterations in Bronchial Epithelial Cells.International journal of molecular sciences · 2021Article
- Transcriptome Sequencing IdentifiesFrontiers in genetics · 2021Article
- HIF-DependentFrontiers in genetics · 2021Article
- Review
- The antiprotease SPINK7 serves as an inhibitory checkpoint for esophageal epithelial inflammatory responses.Science translational medicine · 2018Article
- Impaired response of the bronchial epithelium to inflammation characterizes severe equine asthma.BMC genomics · 2017Article
- TNF is required for TLR ligand-mediated but not protease-mediated allergic airway inflammation.The Journal of clinical investigation · 2017Article
- The differential effects of azithromycin on the airway epithelium in vitro and in vivo.Physiological reports · 2016Article
- Expression of polycomb protein BMI-1 maintains the plasticity of basal bronchial epithelial cells.Physiological reports · 2016Article
- Urokinase plasminogen activator receptor polymorphisms and airway remodelling in asthma.The European respiratory journal · 2016Article
- The Ser82 RAGE Variant Affects Lung Function and Serum RAGE in Smokers and sRAGE Production In Vitro.PloS one · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe asthma-associated gene urokinase plasminogen activator receptor (uPAR) may be involved in epithelial repair and airway remodelling. These processes are not adequately targeted by existing asthma therapies. A fuller understanding of the pathways involved in remodelling may lead to development of new therapeutic opportunities. uPAR expression in the lung epithelium of normal subjects and patients with asthma was investigated and the contribution of uPAR to epithelial wound repair in vitro was studied using primary bronchial epithelial cells (NHBECs).
methodsBronchial biopsy sections from normal subjects and patients with asthma were immunostained for uPAR. NHBECs were used in a scratch wound model to investigate the contribution of the plasminogen pathway to repair. The pathway was targeted via blocking of the interaction between urokinase plasminogen activator (uPA) and uPAR and overexpression of uPAR. The rate of wound closure and activation of intracellular signalling pathways and matrix metalloproteinases (MMPs) were measured.
resultsuPAR expression was significantly increased in the bronchial epithelium of patients with asthma compared with controls. uPAR expression was increased during wound repair in monolayer and air-liquid interface-differentiated NHBEC models. Blocking the uPA-uPAR interaction led to attenuated wound repair via changes in Erk1/2, Akt and p38MAPK signalling. Cells engineered to have raised levels of uPAR showed attenuated repair via sequestration of uPA by soluble uPAR.
conclusionsThe uPAR pathway is required for efficient epithelial wound repair. Increased uPAR expression, as seen in the bronchial epithelium of patients with asthma, leads to attenuated wound repair which may contribute to the development and progression of airway remodelling in asthma. This pathway may therefore represent a potential novel therapeutic target for the treatment of asthma.
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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.