Effect of steroid on hyperoxia-induced ICAM-1 expression in pulmonary endothelial cells

Yukio Suzuki, Kazumi Nishio, Kei Takeshita, Osamu Takeuchi, Kenji Watanabe, Nagato Sato, Katsuhiko Naoki, Hiroyasu Kudo, Takuya Aoki, Kazuhiro Yamaguchi

Research output: Contribution to journalReview articlepeer-review

36 Citations (Scopus)


Intercellular adhesion molecule-1 (ICAM-1) of the vascular endothelium plays a key role in the development of pulmonary oxygen toxicity. We studied the effect of steroid on hyperoxia-induced ICAM-1 expression using cultured endothelial cells in vitro. Human pulmonary artery endothelial cells (HPAECs) were cultured to confluence, and then the monolayers were exposed to either control (21% O2-5% CO2) or hyperoxic (90% O2-5% CO2) conditions with and without a synthetic glucocorticoid, methylprednisolone (MP). MP reduced hyperoxia-induced ICAM-1 and ICAM-1 mRNA expression in a dose-dependent manner. Neutrophil adhesion to hyperoxia-exposed endothelial cells was also inhibited by MP treatment. In addition, MP attenuated hyperoxia-induced H2O2 production in HPAECs as assessed by flow cytometry. An electrophoretic mobility shift assay demonstrated that hyperoxia activated nuclear factor-κB (NF-κB) but not activator protein-1 (AP-1) and that MP attenuated hyperoxia-induced NF-κB activation dose dependently. With Western immunoblot analysis, IκB-α expression was decreased by hyperoxia and increased by MP treatment. These results suggest that MP downregulates hyperoxia-induced ICAM-1 expression by inhibiting NF-κB activation via increased IκB-α expression.

Original languageEnglish
Pages (from-to)L245-L252
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number2 22-2
Publication statusPublished - 2000 Feb


  • Glucocorticoid
  • Inhibitory protein IκB-α
  • Intercellular adhesion molecule-1
  • Nuclear factor-κB

ASJC Scopus subject areas

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


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