Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-kappaB activation in endothelial cells.
Biochim Biophys Acta
; 1783(5): 886-95, 2008 May.
Article
en En
| MEDLINE
| ID: mdl-18241674
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.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Endotelio Vascular
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FN-kappa B
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Especies Reactivas de Oxígeno
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Molécula 1 de Adhesión Intercelular
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Molécula 1 de Adhesión Celular Vascular
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Nicotinamida Fosforribosiltransferasa
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Año:
2008
Tipo del documento:
Article