Hyperoxia-responsive proteins in rat pulmonary microvascular endothelial cells.
Am J Physiol
; 270(4 Pt 1): L517-25, 1996 Apr.
Article
em En
| MEDLINE
| ID: mdl-8928810
ABSTRACT
Exposure to high partial pressures of oxygen are toxic to the lung, and much of the damage observed is related to injury of the pulmonary microvasculature. In this study, we evaluated the response of the pulmonary microvascular endothelial cell to high oxygen concentrations, using two-dimensional protein gel electrophoresis as a direct molecular assay of differences between cells exposed to room air or hyperoxia. We observed a differential expression of five specific proteins within 24 h of a hyperoxic insult that we termed hyperoxia-responsive proteins. After 4 h of hyperoxia there was a decrease in two of the proteins. From 8 to 24 h we observed a repression of a third and an induction of the other two proteins. One of the induced proteins was also increased by heat shock and hydrogen peroxide and has characteristics similar to heat shock protein (HSP) 32 (heme oxygenase 1). Western analysis using an antibody specific to rat heme oxygenase 1 verified that this oxygen-responsive protein is heme oxygenase 1. The response of the other four hyperoxia-responsive proteins appears to be specific to oxygen and not a general stress response, since they were not changed in response to heat shock or hydrogen peroxide. Based on RNA inhibitor and pulse chase experiments, these changes may result from transcriptional/posttranscriptional mechanisms or hyperoxia-dependent protein turnover.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Endotélio Vascular
/
Proteínas
/
Circulação Pulmonar
/
Hiperóxia
Limite:
Animals
Idioma:
En
Revista:
Am J Physiol
Ano de publicação:
1996
Tipo de documento:
Article
País de afiliação:
Estados Unidos