TY - JOUR
T1 - Effect of hyperoxia on adhesion molecule expression in human endothelial cells and neutrophils
AU - Suzuki, Yukio
AU - Aoki, Takuya
AU - Takeuchi, Osamu
AU - Nishio, Kazumi
AU - Suzuki, Kouichi
AU - Miyata, Atsushi
AU - Oyamada, Yoshitaka
AU - Takasugi, Tomoaki
AU - Mori, Masaaki
AU - Fujita, Hirofumi
AU - Yamaguchi, Kazuhiro
PY - 1997/3
Y1 - 1997/3
N2 - 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.
AB - 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.
KW - CD11/CD18
KW - intercellular adhesion molecule- 1
KW - pulmonary oxygen toxicity
KW - reverse transcriptase-polymerase chain reaction
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U2 - 10.1152/ajplung.1997.272.3.l418
DO - 10.1152/ajplung.1997.272.3.l418
M3 - Article
C2 - 9124598
AN - SCOPUS:0348023083
SN - 1040-0605
VL - 272
SP - L418-L425
JO - American Journal of Physiology - Lung Cellular and Molecular Physiology
JF - American Journal of Physiology - Lung Cellular and Molecular Physiology
IS - 3 16-3
ER -