Effect of hyperoxia on adhesion molecule expression in human
endothelial cells and neutrophils.
Suzuki, Yukio, Takuya Aoki, Osamu Takeuchi, Kazumi Nishio, Kouichi
Suzuki, Atsushi Miyata, Yoshitaka Oyamada, Tomoaki Takasugi, Masaaki
Mori, Hirofumi Fujita, and Kazuhiro Yamaguchi.
Department of Internal Medicine and Division of BioMedical
Research, BioMedical Laboratory, Kitasato Institute Hospital, Tokyo
108, Department of Medicine, School of Medicine, Keio University,
Tokyo 160, JAPAN
APStracts 3:0210L, 1996.
To investigate the pathogenesis of pulmonary oxygen toxicity, we
examined the effect of hyperoxia on adhesion molecule expression in
cultured human pulmonary artery (HPAEC) and umbilical vein
endothelial cells (HUVEC). Endothelial cell monolayers were exposed
to either hyperoxic (90% O2, 5% CO2) or normoxic (21% O2, 5% CO2)
conditions for various periods. The level of ICAM-1 expression had
increased in hyperoxia-exposed HPAEC and HUVEC at 48 hours (194 +/-
38% and 233 +/- 56%; p<0.001, respectively) and at 72 hours
(200 +/- 43% and 223 +/- 52%; p<0.001, respectively) as
compared with normoxic conditions. These hyperoxia-induced ICAM-1
expressions were dose-dependently attenuated by a protein kinase C
inhibitor (H-7). In contrast, the levels of P-selectin and E-selectin
expression in HPAEC and HUVEC were unchanged. The levels of ICAM-1
mRNA and the numbers of adherent neutrophils were increased in HPAEC
and HUVEC at 48 hours and at 72 hours of hyperoxia. On the other
hand, hyperoxia caused neutrophil hydrogen peroxide production
without affecting the level of CD11/CD18 expression. These results
suggest that increased ICAM-1 expression in endothelial cells plays
an important role in neutrophil accumulation during hyperoxia.
Received 22 September 1995; accepted in final form 15 October
1996.
APS Manuscript Number L280-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996