Interferon-g Stimulates the Expression of CX3CL1/Fractalkine in Cultured Human Endothelial Cells
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TADAATSU IMAIZUMI, TOMOH MATSUMIYA,1 KOJI FUJIMOTO, KAORI OKAMOTO, XUEFAN CUI, USHIO OHTAKI, HIDEMI YOSHIDA and KEI SATOH
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Department of Vascular Biology, Institute of Brain Science, and 1Department of Dentistry and Oral Surgery, Hirosaki University School of Medicine, Hirosaki 036-8562
CX3CL1/Fractalkine, a CX3C chemokine, is a potent agonist for the chemotaxis and adhesion of monocytes and lymphocytes. It was first identified as a membrane protein in endothelial cells activated with IL-1 or TNF-a. We have found the enhanced expression of fractalkine in human umbilical vein endothelial cells stimulated with interferon-g (IFN-g). Pretreatment of the cells with cycloheximide did not inhibit the expression of fractalkine mRNA. The majority of fractalkine protein was found in the cell lysate, and an antibody-blocking experiment disclosed that fractalkine contributes to the adhesion of mononuclear cells to endothelial monolayers stimulated with IFN-g. Vascular endothelial cells produce fractalkine in response to IFN-g, and this may play an important role in immune responses by eliciting a traffic of mononuclear cells through the vascular wall.
Key words---
fractalkine; endothelial cells; interferon-g
© 2000 Tohoku University Medical Press
Tohoku J. Exp. Med., 2000, 192, 127-139
Address for reprints: Tadaatsu Imaizumi, Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan.
e-mail: timaizum@cc. hirosaki-u.ac.jp
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