ArticleThe American journal of pathology2015
Role of the urokinase-fibrinolytic system in epithelial-mesenchymal transition during lung injury.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 44 citations in OpenAlex.
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- Therapeutic Potential of Lentiviral miR-200a Mimics in Regulating Fibrinolysis and EMT Markers During Pulmonary Fibrosis.FASEB bioAdvances · 2026Article
- p53-miR-34a feedback in lung fibroblasts regulates antifibrotic effects of CSP7, nintedanib, and pirfenidone.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Systemically Administered Anti-uPAR Antibody Plasma and Lung ELF Pharmacokinetics Characterized by Minimal Lung PBPK Model.AAPS PharmSciTech · 2023Article
- PAI-1 regulates AT2-mediated re-alveolarization and ion permeability.Stem cell research & therapy · 2023Article
- Review
- Urokinase System in Pathogenesis of Pulmonary Fibrosis: A Hidden Threat of COVID-19.International journal of molecular sciences · 2023Article
- The Association ofInternational journal of molecular sciences · 2022Article
- Wnt5a/β-catenin axis is involved in the downregulation of AT2 lineage by PAI-1.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Deficiency of Urokinase-Type Plasminogen Activator Receptor Is Associated with the Development of Perivascular Fibrosis in Mouse Heart.Bulletin of experimental biology and medicine · 2022Article
- Article
- Thrombosis and fibrosis: mutually inclusive targets to combat in COVID-19.Future science OA · 2022Article
- H. sinensis mycelium inhibits epithelial-mesenchymal transition by inactivating the midkine pathway in pulmonary fibrosis.Frontiers of medicine · 2021Article
- The Central Role of Fibrinolytic Response in COVID-19-A Hematologist's Perspective.International journal of molecular sciences · 2021Review
- Caveolin-1 scaffolding domain peptide regulates glucose metabolism in lung fibrosis.JCI insight · 2020Article
- Preterm birth and sustained inflammation: consequences for the neonate.Seminars in immunopathology · 2020Review
- Actin is associated with tissue injury in trauma patients and produces a hypercoagulable profile in vitro.The journal of trauma and acute care surgery · 2020Article
- Identification of key modules and hub genes associated with lung function in idiopathic pulmonary fibrosis.PeerJ · 2020Article
- Formulation Composition and Process Affect Counterion for CSP7 Peptide.Pharmaceutics · 2019Article
- Acute Lung Injury: IL-17A-Mediated Inflammatory Pathway and Its Regulation by Curcumin.Inflammation · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Alveolar type II epithelial (ATII) cell injury precedes development of pulmonary fibrosis. Mice lacking urokinase-type plasminogen activator (uPA) are highly susceptible, whereas those deficient in plasminogen activator inhibitor (PAI-1) are resistant to lung injury and pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) has been considered, at least in part, as a source of myofibroblast formation during fibrogenesis. However, the contribution of altered expression of major components of the uPA system on ATII cell EMT during lung injury is not well understood. To investigate whether changes in uPA and PAI-1 by ATII cells contribute to EMT, ATII cells from patients with idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease, and mice with bleomycin-, transforming growth factor β-, or passive cigarette smoke-induced lung injury were analyzed for uPA, PAI-1, and EMT markers. We found reduced expression of E-cadherin and zona occludens-1, whereas collagen-I and α-smooth muscle actin were increased in ATII cells isolated from injured lungs. These changes were associated with a parallel increase in PAI-1 and reduced uPA expression. Further, inhibition of Src kinase activity using caveolin-1 scaffolding domain peptide suppressed bleomycin-, transforming growth factor β-, or passive cigarette smoke-induced EMT and restored uPA expression while suppressing PAI-1. These studies show that induction of PAI-1 and inhibition of uPA during fibrosing lung injury lead to EMT in ATII cells.
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