ArticleAmerican journal of respiratory cell and molecular biology2015
Thrombin down-regulates tissue factor pathway inhibitor expression in a PI3K/nuclear factor-κB-dependent manner in human pleural mesothelial cells.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- 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
- Calponin 1 contributes to myofibroblast differentiation of human pleural mesothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Physical Exercise as a Modulator of Vascular Pathology and Thrombin Generation to Improve Outcomes After Traumatic Brain Injury.Molecular neurobiology · 2022Review
- TGF-β regulation of the uPA/uPAR axis modulates mesothelial-mesenchymal transition (MesoMT).Scientific reports · 2021Article
- NOX1 Promotes Mesothelial-Mesenchymal Transition through Modulation of Reactive Oxygen Species-mediated Signaling.American journal of respiratory cell and molecular biology · 2021Article
- BAY11-7082 inhibits the expression of tissue factor and plasminogen activator inhibitor-1 in type-II alveolar epithelial cells following TNF-α stimulation via the NF-κB pathway.Experimental and therapeutic medicine · 2021Article
- Protease-Activated Receptor-1 Antagonist Protects Against Lung Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2021Article
- Thrombin is a therapeutic target for non-small-cell lung cancer to inhibit vasculogenic mimicry formation.Signal transduction and targeted therapy · 2020Article
- 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
- IKKβ regulates the expression of coagulation and fibrinolysis factors through the NF-κB canonical pathway in LPS-stimulated alveolar epithelial cells type II.Experimental and therapeutic medicine · 2019Article
- Inhibition of Glycogen Synthase Kinase 3β Blocks Mesomesenchymal Transition and Attenuates Streptococcus pneumonia-Mediated Pleural Injury in Mice.The American journal of pathology · 2017Article
- Nuclear factor-kappa B influences early phase of compensatory lung growth after pneumonectomy in mice.Journal of biomedical science · 2017Article
- Precision-guided, Personalized Intrapleural Fibrinolytic Therapy for Empyema and Complicated Parapneumonic Pleural Effusions: The Case for the Fibrinolytic Potential.Clinical pulmonary medicine · 2017Article
- Organizing empyema induced in mice by Streptococcus pneumoniae: effects of plasminogen activator inhibitor-1 deficiency.Clinical and translational medicine · 2016Article
- Tissue factor expression by myeloid cells contributes to protective immune response against Mycobacterium tuberculosis infection.European journal of immunology · 2016Article
- Mesomesenchymal transition of pleural mesothelial cells is PI3K and NF-κB dependent.American journal of physiology. Lung cellular and molecular physiology · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Tissue factor pathway inhibitor (TFPI) is the primary inhibitor of the extrinsic coagulation cascade, and its expression is reported to be relatively stable. Various pathophysiologic agents have been shown to influence TFPI activity by regulating its expression or by modifying the protein. It is not clear how TFPI activity is regulated in normal physiology or in injury. Because thrombin and TFPI are locally elaborated in pleural injury, we sought to determine if thrombin could regulate TFPI in human pleural mesothelial cells (HPMCs). Thrombin significantly decreased TFPI mRNA and protein levels by > 70%. Thrombin-mediated down-regulation of TFPI promoted factor X activation by HPMCs. The ability of thrombin to significantly decrease TFPI mRNA and protein levels was maintained at nanomolar concentrations. Protease-activated receptor (PAR)-1, a mediator of thrombin signaling, is detectable in the mesothelium in human and murine pleural injury. PAR-1 silencing blocked thrombin-mediated decrements of TFPI in HPMCs. Thrombin activates PI3K/Akt and nuclear factor κB (NF-κB) signaling in HPMCs. Inhibition of PI3K (by PX-866) and NF-κB (by SN50) prevented thrombin-mediated TFPI mRNA and protein down-regulation. These are the first studies to demonstrate that thrombin decreases TFPI expression in HPMCs. Our findings demonstrate a novel mechanism by which thrombin regulates TFPI expression in HPMCs and promotes an unrestricted procoagulant response, and suggest that interactions between PI3K and NF-κB signaling pathways are linked in HPMCs and control TFPI expression. These findings raise the possibility that targeting this pathway could limit the ability of the mesothelium to support extravascular fibrin deposition and organization associated with pleural injury.
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