Abstract

The normal balance between coagulation and fibrinolysis in the lung is disrupted in acute lung injury syndromes, such as adult and neonatal respiratory distress syndromes (ARDS and RDS), leading to widespread interstitial and broncho-alveolar fibrin deposition. Persistence of the fibrin deposits has been associated with the development of pulmonary fibrosis and bronchopulmonary dysplasia (BPD). Procoagulant activity in lung is due to tissue factor (TF) and fibrinolytic activity is due to urokinase-type plasminogen activator (uPA) produced by alveolar epithelial cells. We have previously demonstrated that dexamethasone (dex) induces TF mRNA and protein in HFL. In this study we characterized the effect of dex) on uPA mRNA in a HFL explant culture system using RT-PCR and RNAse protection assay.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.