Hyperoxia-responsive proteins in rat pulmonary microvascular
endothelial cells.
Visner, Gary A., Sandra Fogg, and Harry S. Nick.
Departments of Pediatrics and Biochemistry and Molecular Biology,
University of Florida, Gainesville, FL 32610
APStracts 2:0204L, 1995.
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, utilizing 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 5
specific proteins within 24 h of an hyperoxic insult which we termed
hyperoxia-responsive proteins. Following 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 HSP 32 (heme oxygenase
1). Western analysis utilizing an antibody specific to rat heme
oxygenase 1 verified that this oxygen responsive protein is heme
oxygenase 1. The response of the other 4 hyperoxia-responsive
proteins appear 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/post
-transcriptional mechanisms or hyperoxia-dependent protein turnover.
Received 27 July 1994; accepted in final form 1 October 1995.
APS Manuscript Number L211-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95