| First Author | Piedboeuf B | Year | 1998 |
| Journal | Am J Respir Cell Mol Biol | Volume | 19 |
| Issue | 4 | Pages | 543-53 |
| PubMed ID | 9761750 | Mgi Jnum | J:51594 |
| Mgi Id | MGI:1321012 | Doi | 10.1165/ajrcmb.19.4.2349 |
| Citation | Piedboeuf B, et al. (1998) Increased endothelial cell expression of platelet-endothelial cell adhesion molecule-1 during hyperoxic lung injury. Am J Respir Cell Mol Biol 19(4):543-53 |
| abstractText | 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. |
