ArticleAmerican journal of respiratory cell and molecular biology2014
Plasminogen activator inhibitor-1 deficiency augments visceral mesothelial organization, intrapleural coagulation, and lung restriction in mice with carbon black/bleomycin-induced pleural injury.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 43 citations in OpenAlex.
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- The Role of Tuftelin-1 in Mesomesenchymal Transition of Pleural Mesothelial Cells and the Progression of Pleural Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Myocardin regulates fibronectin expression and secretion from human pleural mesothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Bacteriophage therapy for the treatment of Mycobacterium tuberculosis infections in humanized mice.Communications biology · 2024Article
- A Novel Humanized Mouse Model for HIV and Tuberculosis Co-infection Studies.bioRxiv : the preprint server for biology · 2024Article
- Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- The mTORC2/SGK1/NDRG1 Signaling Axis Is Critical for the Mesomesenchymal Transition of Pleural Mesothelial Cells and the Progression of Pleural Fibrosis.American journal of respiratory cell and molecular biology · 2024Article
- A novel humanized mouse model for HIV and tuberculosis co-infection studies.Frontiers in immunology · 2024Article
- Bottlebrush inspired injectable hydrogel for rapid prevention of postoperative and recurrent adhesion.Bioactive materials · 2022Article
- Myo5b Transports Fibronectin-Containing Vesicles and Facilitates FN1 Secretion from Human Pleural Mesothelial Cells.International journal of molecular sciences · 2022Article
- Early IL-17A production helps establish Mycobacterium intracellulare infection in mice.PLoS pathogens · 2022Article
- Calponin 1 contributes to myofibroblast differentiation of human pleural mesothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- DOCK2 Promotes Pleural Fibrosis by Modulating Mesothelial to Mesenchymal Transition.American journal of respiratory cell and molecular biology · 2022Article
- Update on Novel Targeted Therapy for Pleural Organization and Fibrosis.International journal of molecular sciences · 2022Review
- TGF-β regulation of the uPA/uPAR axis modulates mesothelial-mesenchymal transition (MesoMT).Scientific reports · 2021Article
- Endothelial Cell Protein C Receptor Deficiency AttenuatesAmerican journal of respiratory cell and molecular biology · 2021Article
- NOX1 Promotes Mesothelial-Mesenchymal Transition through Modulation of Reactive Oxygen Species-mediated Signaling.American journal of respiratory cell and molecular biology · 2021Article
- Primary human mesothelial cell culture in the evaluation of the inflammatory response to different sclerosing agents used for pleurodesis.Physiological reports · 2021Article
- The Contribution of the Urokinase Plasminogen Activator and the Urokinase Receptor to Pleural and Parenchymal Lung Injury and Repair: A Narrative Review.International journal of molecular sciences · 2021Review
- Glycogen Synthase Kinase-3β Inhibition with 9-ING-41 Attenuates the Progression of Pulmonary Fibrosis.Scientific reports · 2019Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Local derangements of fibrin turnover and plasminogen activator inhibitor (PAI)-1 have been implicated in the pathogenesis of pleural injury. However, their role in the control of pleural organization has been unclear. We found that a C57Bl/6j mouse model of carbon black/bleomycin (CBB) injury demonstrates pleural organization resulting in pleural rind formation (14 d). In transgenic mice overexpressing human PAI-1, intrapleural fibrin deposition was increased, but visceral pleural thickness, lung volumes, and compliance were comparable to wild type. CBB injury in PAI-1(-/-) mice significantly increased visceral pleural thickness (P < 0.001), elastance (P < 0.05), and total lung resistance (P < 0.05), while decreasing lung compliance (P < 0.01) and lung volumes (P < 0.05). Collagen, α-smooth muscle actin, and tissue factor were increased in the thickened visceral pleura of PAI-1(-/-) mice. Colocalization of α-smooth muscle actin and calretinin within pleural mesothelial cells was increased in CBB-injured PAI-1(-/-) mice. Thrombin, factor Xa, plasmin, and urokinase induced mesothelial-mesenchymal transition, tissue factor expression, and activity in primary human pleural mesothelial cells. In PAI-1(-/-) mice, D-dimer and thrombin-antithrombin complex concentrations were increased in pleural lavage fluids. The results demonstrate that PAI-1 regulates CBB-induced pleural injury severity via unrestricted fibrinolysis and cross-talk with coagulation proteases. Whereas overexpression of PAI-1 augments intrapleural fibrin deposition, PAI-1 deficiency promotes profibrogenic alterations of the mesothelium that exacerbate pleural organization and lung restriction.
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