title: Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-kappaB activation in endothelial cells.
abstract: Visfatin has recently been identified as a novel visceral adipokine which may be involved in obesity-related vascular disorders. However, it is not known whether visfatin directly contributes to endothelial dysfunction. Here, we investigated the effect of visfatin on vascular inflammation, a key step in a variety of vascular diseases. Visfatin induced leukocyte adhesion to endothelial cells and the aortic endothelium by induction of the cell adhesion molecules, ICAM-1 and VCAM-1. Promoter analysis revealed that visfatin-mediated induction of CAMs is mainly regulated by nuclear factor-kappaB (NF-kappaB). Visfatin stimulated IkappaBalpha phosphorylation, nuclear translocation of the p65 subunit of NF-kappaB, and NF-kappaB DNA binding activity in HMECs. Furthermore, visfatin increased ROS generation, and visfatin-induced CAMs expression and NF-kappaB activation were abrogated in the presence of the direct scavenger of ROS. Taken together, our results demonstrate that visfatin is a vascular inflammatory molecule that increases expression of the inflammatory CAMs, ICAM-1 and VCAM-1, through ROS-dependent NF-kappaB activation in endothelial cells.
authors.affiliation: School of Dentistry, Pusan National University, Pusan, South Korea.
authors.forename: Su-Ryun
authors.initials: SR
authors.lastname: Kim
authors.forename: Yun-Hee
authors.initials: YH
authors.lastname: Bae
authors.forename: Soo-Kyung
authors.initials: SK
authors.lastname: Bae
authors.forename: Kyu-Sil
authors.initials: KS
authors.lastname: Choi
authors.forename: Kwon-Ha
authors.initials: KH
authors.lastname: Yoon
authors.forename: Tae Hyeon
authors.initials: TH
authors.lastname: Koo
authors.forename: Hye-Ock
authors.initials: HO
authors.lastname: Jang
authors.forename: Il
authors.initials: I
authors.lastname: Yun
authors.forename: Kyu-Won
authors.initials: KW
authors.lastname: Kim
authors.forename: Young-Guen
authors.initials: YG
authors.lastname: Kwon
authors.forename: Mi-Ae
authors.initials: MA
authors.lastname: Yoo
authors.forename: Moon-Kyoung
authors.initials: MK
authors.lastname: Bae
mesh_terms: D002448:Cell Adhesion; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D015870:Gene Expression; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism; D007962:Leukocytes / Q000276:immunology; D019255:NADPH Oxidases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism*; D054409:Nicotinamide Phosphoribosyltransferase / Q000494:pharmacology*; D011401:Promoter Regions, Genetic; D017382:Reactive Oxygen Species / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism
chemical_list: D016328:NF-kappa B; D017382:Reactive Oxygen Species; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019255:NADPH Oxidases; D054409:Nicotinamide Phosphoribosyltransferase