Hypoxia/reoxygenation stimulates Ca 2+-dependent ICAM-1 mRNA expression in human aortic endothelial cells

Roy C. Ziegelstein, Chaoxia He, Qinghua Hu

Research output: Contribution to journalArticlepeer-review

Abstract

Increased endothelial ICAM-1 expression is found in normal aging and in atherosclerosis and is related to the chronic effects of oxidative stress. We examined the Ca 2+-dependence of ICAM-1 mRNA expression in human aortic endothelial cells (HAEC) exposed to hypoxia/reoxygenation (H/R) as a model of oxidative stress. HAEC were exposed to glucose-free hypoxia (95% N 2/5% CO 2) for 60 min and were then reoxygenated (21% O 2/5% CO 2) and observed for up to 6 h. Reactive oxygen species (ROS) generation was measured by dichlorofluorescein fluorescence and ICAM-1 mRNA was assessed by Northern blot. Upon reoxygenation after hypoxia, ROS production occurred in HAEC and was inhibited by diphenyleneiodonium and by polyethylene glycol-catalase, suggesting the involvement of NADPH oxidase-derived hydrogen peroxide. Hypoxia alone did not increase either ROS production or ICAM-1 mRNA levels, but a 2.5-fold increase in ICAM-1 mRNA was noted by 30 min of reoxygenation. This was not observed in Ca 2+-free buffer or in cells treated with diphenyleneiodonium. Thus, H/R upregulates ICAM-1 mRNA in HAEC by a Ca 2+- and ROS-dependent mechanism. Characterizing the signaling pathways involved in H/R-induced adhesion molecule expression may result in a better understanding of the vascular biology of normal aging and the pathobiology of atherosclerosis.

Original languageEnglish (US)
Pages (from-to)68-73
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume322
Issue number1
DOIs
StatePublished - Sep 10 2004

Keywords

  • Aging
  • Atherosclerosis
  • Calcium (cellular)
  • Hypoxia/anoxia
  • ICAM-1
  • Redox signaling
  • Reoxygenation

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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