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Articles in PresS, published online ahead of print March 15, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00451.2001
Submitted on November 20, 2001
Accepted on March 8, 2002
1 Medicine, Johns Hopkins University, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: wagnerem{at}jhmi.edu.
In vivo models of airway inflammation suggest that most protein transudation occurs from the bronchial microcirculation. However, due to technical limitations in the isolation and culture of bronchial endothelial cells, most studies of lung vascular permeability have focused on pulmonary endothelium. Thus, conditions for culture of sheep bronchial artery(BAEC) and bronchial microvascular endothelial cells (BMVEC)were established. The bronchial artery and the mainstem bronchi stripped of epithelium were dissected and endothelial cells were isolated by enzymatic treatment. BAEC and BMVEC demonstrated positive staining for factor VIII-related antigen, DiI-Ac-LDL and PECAM-1. Radioligand binding studies confirmed equivalent numbers of B2 kinin receptors on BAEC and BMVEC. Permeability of BAEC and BMVEC was determined after treatment with bradykinin and thrombin by comparing the translocation of FITCdextran (9,500 MW) across confluent monolayers (n=10-12). Bradykinin caused a maximal increase in permeability in BAEC(165% increase) and BMVEC(144% increase)by 15 min compared to vehicle controls. Thrombin treatment altered BMVEC permeability only, reaching a maximal response at 60 min(109% increase). These results demonstrate bronchial endothelial cell heterogeneity and establish methods to determine intracellular mechanisms contributing to airway disease in relevant cell systems.
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