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      Effect of hypoxia on the expression of fractalkine in human endothelial cells.

      The Tohoku journal of experimental medicine

      metabolism, Acetylcysteine, pharmacology, Cell Hypoxia, Cells, Cultured, Chemokine CX3CL1, Chemokines, CX3C, genetics, Deferoxamine, Endothelial Cells, cytology, drug effects, Endothelium, Vascular, Humans, Interferon-gamma, Iron Chelating Agents, Membrane Proteins, Oxygen, RNA, Messenger, Vascular Endothelial Growth Factor A

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          CX3CL1/fractalkine is a chemokine with a unique CX3C motif. Hypoxia mediates the expression of various genes, such as vascular endothelial growth factor (VEGF), cyclooxygenase-2, and plasminogen-activator inhibitor-1, in vascular endothelial cells. We studied the effect of hypoxia on the expression of fractalkine induced by interferon-gamma (IFN-gamma) in endothelial cells. Human umbilical vein endothelial cells were cultured, and the stimulation of the cells with IFN-gamma was found to induce the expression of fractalkine. Hypoxia inhibited the expression of fractalkine mRNA and protein by IFN-gamma, and this effect was observed with concomitant increase in VEGF expression. Desferrioxamine, an iron chelator that mimics hypoxia in vitro, also inhibited the fractalkine production induced by IFN-gamma. Hypoxia did not affect the degradation of fractalkine mRNA. The inhibition of fractalkine expression by hypoxia was reversed on returning the cultures to reoxygenation condition. Inhibition of IFN-induced fractalkine expression by hypoxia was not affected by the presence of a radical scavenger, N-acetyl-L-cysteine, and the involvement of reactive oxygen species may be excluded. Inhibition of fractalkine expression by hypoxia may be involved in the pathophysiology of ischemic diseases.

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