Effect of hyperoxia on adhesion molecule expression in human endothelial cells and neutrophils

Yukio Suzuki, Takuya Aoki, Osamu Takeuchi, Kazumi Nishio, Kouichi Suzuki, Atsushi Miyata, Yoshitaka Oyamada, Tomoaki Takasugi, Masaaki Mori, Hirofumi Fujita, Kazuhiro Yamaguchi

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)


To investigate the pathogenesis of pulmonary oxygen toxicity, we examined the effect of hyperoxia on adhesion molecule expression in cultured human pulmonary artery endothelial cells (HPAEC) and human 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 intercellular adhesion molecule (ICAM)-1 expression had increased in hyperoxia-exposed HPAEC and HUVEC at 48 h (194 ± 38 and 233 ± 56%, respectively; P < 0.001) and at 72 h (200 ± 43 and 223 ± 52%, respectively; P < 0.001) 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 and 72 h of hyperoxia. On the other hand, hyperoxia caused neutrophil H2O2 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.

Original languageEnglish
Pages (from-to)L418-L425
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number3 16-3
Publication statusPublished - 1997 Mar


  • CD11/CD18
  • intercellular adhesion molecule- 1
  • pulmonary oxygen toxicity
  • reverse transcriptase-polymerase chain reaction

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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