ICAM-1 expression and cellular injury in cultured endothelial cells under hypoxia/reoxygenation.
Intercellular adhesion molecule 1(ICAM-1) expression and cellular changes in human umbilical vein endothelial cells(HUVEC) and ECV304, an established cultured line derived from HUVEC, under hypoxia and hypoxia(H)/reoxygenation(R) were investigated by immunological, cytochemical, and morphological methods. ICAM-1 expression in HUVEC decreased slightly under hypoxia(92%) and was up-regulated under reoxygenation(114%), but this up-regulation was diminished by superoxide dismutase(SOD). The up-regulation of ICAM-1 expression by interleukin-1 beta(IL-1 beta) was detected at almost equal levels under hypoxia, and H/R. Using lucigenin-chemiluminescence, we demonstrated superoxide generation from HUVEC under H/R. The Ca2+ influx under hypoxia, and the Ca2+ release from the cells under H/R reduced by SOD were detected cytochemically. Vacuole formation as cell injury under hypoxia and H/R was detected by electron microscopy. The present findings provide evidence that superoxide generated from HUVEC is responsible for the up-regulation of ICAM-1 expression under H/R, and the cause of endothelial cellular injury.
Mataki
H
H
Department of Internal Medicine, Kobe University School of Medicine.
Inagaki
T
T
Yokoyama
M
M
Maeda
S
S
D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*
D018799:Intercellular Adhesion Molecule-1; D010100:Oxygen