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Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-κB activation in endothelial cells

2008; Elsevier BV; Volume: 1783; Issue: 5 Linguagem: Inglês

10.1016/j.bbamcr.2008.01.004

1879-2596

Su-Ryun Kim, Yun-Hee Bae, Soo-Kyung Bae, Kyu-Sil Choi, Kwon‐Ha Yoon, Tae Hyeon Koo, Hye-Ock Jang, Il Yun, Kyu-Won Kim, Young‐Guen Kwon, Mi‐Ae Yoo, Moon-Kyoung Bae,

Antioxidant Activity and Oxidative Stress

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-κB (NF-κB). Visfatin stimulated IκBα phosphorylation, nuclear translocation of the p65 subunit of NF-κB, and NF-κB DNA binding activity in HMECs. Furthermore, visfatin increased ROS generation, and visfatin-induced CAMs expression and NF-κB 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-κB activation in endothelial cells.