Am. J. Respir. Cell Mol. Biol., Volume 19, Number 4, October, 1998 543-553

Increased Endothelial Cell Expression of Platelet-Endothelial Cell Adhesion Molecule-1 during Hyperoxic Lung Injury

Bruno Piedboeuf, Marie Gamache, Johanne Frenette, Stuart Horowitz, H. Scott Baldwin, and Peter Petrov

Department of Pediatrics, Centre de Recherche du CHUL, Centre Hospitalier Universitaire de Québec, Sainte Foy, Québec, Canada; CardioPulmonary Research Institute, Winthrop-University Hospital, The State University of New York at Stony Brook, Mineola, New York; and the Cardiology Division, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania

Lung injury is a frequent consequence of oxygen (O₂) therapy administered to newborns and adults with respiratory distress. Acute exposure to hyperoxia results in a well-described pathophysiologic response in the lungs. Because inflammation is an important component of pulmonary O₂ toxicity, we have an interest in identifying the inflammatory mediators that increase during hyperoxia. Platelet-endothelial cell adhesion molecule-1 (PECAM-1), a member of the immunoglobulin superfamily that is expressed at the junctions between endothelial cells, is essential to the transendothelial migration of leukocytes. We hypothesized that increased expression of PECAM-1 occurs in pulmonary endothelial cells during hyperoxic lung injury. Adult mice were exposed to 100% O₂ for up to 96 h. We analyzed PECAM-1 expression by RNA blot hybridization, in situ hybridization, and immunohistochemistry. A increase in PECAM-1 mRNA was seen as soon as 2 d of hyperoxia relative to unexposed control mice. PECAM-1 mRNA and protein were found in endothelial cells of both large and small arteries. The expression of PECAM-1 in capillary vessels was further confirmed using in situ hybridization at the electron microscope level. This increase in PECAM-1 expression coincided with the appearance of leukocytes in lung tissue. These observations suggest that PECAM-1 expression is a relatively early step in the inflammation cascade, and intervention at this phase may be critical to the prevention of further damage.

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