The Tohoku Journal of Experimental Medicine
Online ISSN : 1349-3329
Print ISSN : 0040-8727
Regular Contributions
Effect of Hypoxia on the Expression of Fractalkine in Human Endothelial Cells
Koji YamashitaTadaatsu ImaizumiMasaharu HatakeyamaWakako TamoDaisuke KimuraMika KumagaiHidemi YoshidaKei Satoh
Author information
JOURNALS FREE ACCESS

2003 Volume 200 Issue 4 Pages 187-194

Details
Abstract

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 eect of hypoxia on the expression of fractalkine induced by interferon-γ (IFN-γ) in endothelial cells. Human umbilical vein endothelial cells were cultured, and the stimulation of the cells with IFN-γ was found to induce the expression of fractalkine. Hypoxia inhibited the expression of fractalkine mRNA and protein by IFN-γ, and this eect 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-γ. Hypoxia did not aect 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 aected 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.

Information related to the author
© 2003 Tohoku University Medical Press
Previous article Next article
feedback
Top