ArticleAmerican journal of respiratory cell and molecular biology2015
Targeting of plasminogen activator inhibitor 1 improves fibrinolytic therapy for tetracycline-induced pleural injury in rabbits.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Optimized TELIP, an Echogenic Liposomal Nano-Carrier Loaded with Alteplase for Preclinical Studies.Pharmaceutics · 2026Article
- Review
- INHIBITING THE INHIBITOR: WOULD TARGETING PAI-1 RESULT IN A LOW-DOSE, WELL-TOLERATED TREATMENT OF EMPYEMA?Biomedical sciences instrumentation · 2025Article
- Research Priorities for Malignant Pleural Organization with Loculation and Failed Drainage.Cells · 2025Review
- Pleural Infection: Diagnosis, Management, and Future Directions.Journal of clinical medicine · 2025Review
- Intrapleural Fibrinolytic Interventions for Retained Hemothoraces in Rabbits.International journal of molecular sciences · 2024Article
- Targeting the PAI-1 Mechanism with a Small Peptide Increases the Efficacy of Alteplase in a Rabbit Model of Chronic Empyema.Pharmaceutics · 2023Article
- PAI-1 Drives Septation and Clinical Outcomes in Pleural Infection.American journal of respiratory and critical care medicine · 2023Article
- Precision targeting of the plasminogen activator inhibitor-1 mechanism increases efficacy of fibrinolytic therapy in empyema.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
- From Bedside to the Bench-A Call for Novel Approaches to Prognostic Evaluation and Treatment of Empyema.Frontiers in pharmacology · 2021Review
- Structural Insights into the Mechanism of a Nanobody That Stabilizes PAI-1 and Modulates Its Activity.International journal of molecular sciences · 2020Article
- Molecular mechanism of two nanobodies that inhibit PAI-1 activity reveals a modulation at distinct stages of the PAI-1/plasminogen activator interaction.Journal of thrombosis and haemostasis : JTH · 2020Article
- Acute Lung Injury: IL-17A-Mediated Inflammatory Pathway and Its Regulation by Curcumin.Inflammation · 2019Review
- Phase 1 trial of intrapleural LTI-01; single chain urokinase in complicated parapneumonic effusions or empyema.JCI insight · 2019Article
- Lack of durable protection against cotton smoke-induced acute lung injury in sheep by nebulized single chain urokinase plasminogen activator or tissue plasminogen activator.Clinical and translational medicine · 2018Article
- Fibrin turnover and pleural organization: bench to bedside.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- Targeting plasminogen activator inhibitor-1 in tetracycline-induced pleural injury in rabbits.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Precision-guided, Personalized Intrapleural Fibrinolytic Therapy for Empyema and Complicated Parapneumonic Pleural Effusions: The Case for the Fibrinolytic Potential.Clinical pulmonary medicine · 2017Article
- Dose dependency of outcomes of intrapleural fibrinolytic therapy in new rabbit empyema models.American journal of physiology. Lung cellular and molecular physiology · 2016Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Endogenous active plasminogen activator inhibitor 1 (PAI-1) was targeted in vivo with monoclonal antibodies (mAbs) that redirect its reaction with proteinases to the substrate branch. mAbs were used as an adjunct to prourokinase (single-chain [sc] urokinase [uPA]) intrapleural fibrinolytic therapy (IPFT) of tetracycline-induced pleural injury in rabbits. Outcomes of scuPA IPFT (0.25 or 0.0625 mg/kg) with 0.5 mg/kg of mouse IgG or mAbs (MA-33H1F7 and MA-8H9D4) were assessed at 24 hours. Pleural fluid (PF) was collected at 0, 10, 20, and 40 minutes and 24 hours after IPFT and analyzed for plasminogen activating (PA), uPA, fibrinolytic activities, levels of total plasmin/plasminogen, α-macroglobulin (αM), mAbs/IgG antigens, free active uPA, and αM/uPA complexes. Anti-PAI-1 mAbs, but not mouse IgG, delivered with an eightfold reduction in the minimal effective dose of scuPA (from 0.5 to 0.0625 mg/kg), improved the outcome of IPFT (P < 0.05). mAbs and IgG were detectable in PFs at 24 hours. Compared with identical doses of scuPA alone or with IgG, treatment with scuPA and anti-PAI-1 mAbs generated higher PF uPA amidolytic and PA activities, faster formation of αM/uPA complexes, and slower uPA inactivation. However, PAI-1 targeting did not significantly affect intrapleural fibrinolytic activity or levels of total plasmin/plasminogen and αM antigens. Targeting PAI-1 did not induce bleeding, and rendered otherwise ineffective doses of scuPA able to improve outcomes in tetracycline-induced pleural injury. PAI-1-neutralizing mAbs improved IPFT by increasing the durability of intrapleural PA activity. These results suggest a novel, well-tolerated IPFT strategy that is tractable for clinical development.
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