ArticleVascular pharmacology2018
Attenuation of murine acute lung injury by PF-573,228, an inhibitor of focal adhesion kinase.
Article in Vascular pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Multifactorial pathogenesis of rheumatoid arthritis: interaction between inflammation, metabolic dysregulation, and tissue mechanics.Frontiers in immunology · 2026Review
- Targeting Focal Adhesion Kinase in Lung Diseases: Current Progress and Future Directions.Biomolecules · 2025Review
- Focal adhesion kinase (FAK): emerging target for drug-resistant malignant tumors.Molecular biology reports · 2025Review
- [Protective effect of FAK inhibitor PF-562271 against human umbilical vein endothelial cell injury induced by aging platelets].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Carvedilol alleviates lipopolysaccharide (LPS)-induced acute lung injury by inhibiting Ras homolog family member A (RhoA)/ROCK activities.Bioengineered · 2022Article
- Isoalantolactone inhibits pancreatic cancer proliferation by regulation of PI3K and Wnt signal pathway.PloS one · 2021Article
- Nur77 limits endothelial barrier disruption to LPS in the mouse lung.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Heat Shock Protein 27 Phosphorylation Regulates Tumor Cell Migration under Shear Stress.Biomolecules · 2019Article
- Cortical Actin Dynamics in Endothelial Permeability.Current topics in membranes · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Acute lung injury (ALI) is characterized by endothelial barrier disruption resulting in increased vascular permeability. As focal adhesion kinase (FAK), a non-receptor protein tyrosine kinase, is involved in endothelial cell (EC) barrier regulation, we hypothesized that FAK inhibition could attenuate agonist-induced EC barrier disruption relevant to ALI. Human lung EC were pretreated with one of three pharmacologic FAK inhibitors, PF-573,228 (PF-228, 10 μM), PF-562,271 (PF-271, 5 μM) or NVP-TAE226 (TAE226, 5 μM) for 30 min prior to treatment with thrombin (1 U/ml, 30 min). Western blotting confirmed attenuated thrombin-induced FAK phosphorylation associated with all three inhibitors. Subsequently, EC were pretreated with either PF-228 (10 μM), TAE226 (5 μM) or PF-271 (5 μM) for 30 min prior to thrombin stimulation (1 U/ml) followed by measurements of barrier integrity by transendothelial electrical resistance (TER). Separately, EC grown in transwell inserts prior to thrombin (1 U/ml) with measurements of FITC-dextran flux after 30 min confirmed a significant attenuation of thrombin-induced EC barrier disruption by PF-228 alone. Finally, in a murine ALI model induced by LPS (1.25 mg/ml, IT), rescue treatment with PF-228 was associated with significantly reduced lung injury. Our findings PF-228, currently being studied in clinical trials, may serve as a novel and effective therapeutic agent for ALI.
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