ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Mesomesenchymal transition of pleural mesothelial cells is PI3K and NF-κB dependent.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 35 citations in OpenAlex.
- Upregulated CCN1 from pleural mesothelial cells alters collagen I conformation and drives fibrosis via ITGB1/MAPK signaling.Cellular & molecular biology letters · 2026Article
- Extracellular Vesicles Contribute to the Pathophysiology and Progression of Pleural Fibrosis by Promoting Mesothelial-to-Mesenchymal Transition and Neoangiogenesis.American journal of respiratory cell and molecular biology · 2025Article
- 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
- Causal effect of gut microbiota on the risk of cancer and potential mediation by inflammatory proteins.World journal of surgical oncology · 2025Article
- Myocardin regulates fibronectin expression and secretion from human pleural mesothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Pleural Fibrosis: Now That's What mTORC(ing) About.American journal of respiratory cell and molecular biology · 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
- Plasminogen Binding and Activation at the Mesothelial Cell Surface Promotes Invasion through a Collagen Matrix.International journal of molecular sciences · 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
- Insights from DOCK2 in cell function and pathophysiology.Frontiers in molecular biosciences · 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
- 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
- Thrombin Upregulates PAI-1 and Mesothelial-Mesenchymal Transition Through PAR-1 and Contributes to Tuberculous Pleural Fibrosis.International journal of molecular sciences · 2019Article
- Myocardin Is Involved in Mesothelial-Mesenchymal Transition of Human Pleural Mesothelial Cells.American journal of respiratory cell and molecular biology · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Pleural organization follows acute injury and is characterized by pleural fibrosis, which may involve the visceral and parietal pleural surfaces. This process affects patients with complicated parapneumonic pleural effusions, empyema, and other pleural diseases prone to pleural fibrosis and loculation. Pleural mesothelial cells (PMCs) undergo a process called mesothelial mesenchymal transition (MesoMT), by which PMCs acquire a profibrotic phenotype characterized by cellular enlargement and elongation, increased expression of α-smooth muscle actin (α-SMA), and matrix proteins including collagen-1. Although MesoMT contributes to pleural fibrosis and lung restriction in mice with carbon black/bleomycin-induced pleural injury and procoagulants and fibrinolytic proteases strongly induce MesoMT in vitro, the mechanism by which this transition occurs remains unclear. We found that thrombin and plasmin potently induce MesoMT in vitro as does TGF-β. Furthermore, these mediators of MesoMT activate phosphatidylinositol-3-kinase (PI3K)/Akt and NF-κB signaling pathways. Inhibition of PI3K/Akt signaling prevented TGF-β-, thrombin-, and plasmin-mediated induction of the MesoMT phenotype exhibited by primary human PMCs. Similar effects were demonstrated through blockade of the NF-κB signaling cascade using two distinctly different NF-κB inhibitors, SN50 and Bay-11 7085. Conversely, expression of constitutively active Akt-induced mesenchymal transition in human PMCs whereas the process was blocked by PX866 and AKT8. Furthermore, thrombin-mediated MesoMT is dependent on PAR-1 expression, which is linked to PI3K/Akt signaling downstream. These are the first studies to demonstrate that PI3K/Akt and/or NF-κB signaling is critical for induction of MesoMT.
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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.