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Induction of fractalkine by endothelial cells under shear stress.

Atherosclerotic lesions show a focal pattern of distribution in the arterial tree, in which they have a predilection in regions such as bends and bifurcations where the wall shear stress is low and there might be disruption in the laminar flow pattern [1]. Different studies have shown that low shear stress is associated with the appearance of leukocyte adhesion molecules on the surface of the endothelial cells, and with leukocyte transmigration [2]. Fractalkine (FKN) is a novel and unique chemokine that exists in both a soluble form and in a membrane-anchored form. FKN mediates both firm adhesion of leukocytes to the endothelium and leukocyte transmigration to extravascular target tissues, via its seven-transmembrane domain G-protein-coupled receptor CX3CR1. Moreover, FKN is upregulated on inflamed endothelium that can function as a chemoattractant and as a direct adhesin via CX3CR1 [3]. We have previously reported that CX3CR1 may participate in the pathogenesis of atherosclerosis by a CX3CR1 mutation affecting fractalkine-mediated inflammatory events [4].