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First published on April 13, 2006; DOI: 10.1124/mol.106.022392

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Received for publication January 11, 2006.
Revised April 13, 2006.
Accepted for publication April 13, 2006.

Resveratrol Suppresses TNF-{alpha}-Induced Fractalkine Expression in Endothelial Cells

Sang Ok Moon 1, Won Kim 1, Mi Jeong Sung 1, Sik Lee 1, Kyung Pyo Kang 1, Duk Hoon Kim 1, Sang Yong Lee 1, Jun No So 1, Sung Kwang Park 1*

1 Chonbuk National University Medical School

* Address correspondence to: E-mail: parksk{at}chonbuk.ac.kr

Abstract

Up-regulation of fractalkine is involved in vascular and tissue damage in inflammatory conditions. Resveratrol has been shown to have anti-inflammatory, antioxidant, and antitumor activities. Its regulatory effects on expression of fractalkine in vascular endothelial cells and fractalkine receptor, CX3CR1 in monocytes have not been studied. We evaluated the effects of resveratrol on fractalkine expression in human umbilical vein endothelial cells and CX3CR1 expression in THP-1 cells in response to treatment with tumor necrosis factor (TNF)-{alpha}. TNF-{alpha} significantly induced fractalkine mRNA and protein expression in endothelial cells. Resveratrol strongly suppressed TNF-{alpha}-induced fractalkine expression in endothelial cells through suppression of nuclear factor-{kappa}B and Sp1 activities. Resveratrol decreased the number of TNF-{alpha}-induced fractalkine-positive endothelial cells and CX3CR1-positive cells determined by flow cytometric analysis. Resveratrol suppressed TNF-{alpha}-stimulated monocytes adhesion to human umbilical vein endothelial cells. Immunohistochemical analysis revealed that resveratrol suppressed TNF-{alpha}-induced arterial endothelial fractalkine expression in heart, kidney, and intestine and decreased ED-1-positive cell infiltration in intestinal villi. Resveratrol may provide a new pharmacological approach for suppressing fractalkine/CX3CR1-mediated injury in inflammatory conditions.


Key words: Tumor necrosis factor, Leukocytes/Mast cells


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