VASCULAR

Full list of author information is available at the end of the articleIntroduction Vascular inflammation is a primary event in the patho-genesis of many human diseases, including atheros-clerosis, hypertension, and restenosis [1-3]. The vascular inflammatory reaction is mediated by complex interac-tions between circulating leukocytes and the endothe-lium. Activation of endothelial cells by proinflammatory molecules, including tumor necrosis factor α (TNFα), in-creases the expression of adhesion molecules and the ad-hesion of leukocytes to the vascular endothelium, which are critical steps in the initiation of atherosclerosis [4]. Vascular adhesion molecules are critical for the initiation and progression of atherosclerosis [5]. The transcription factor nuclear factor-κB (NF-κB) is in-volved in a wide variety of phenomena, including athero-scleorosis [6]. Activated NF-κB has been identified in situ in human atherosclerotic plaques [7,8]. A number of genes of which the products have been implicated in the de-velopment of atherosclerosis are regulated by NF-κB. Various leukocyte adhesion molecules, such as intracel-lular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin, as well as vari-ous chemokines such as monocyte chemoattractan