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.
|Number of pages||10|
|Journal||Biochimica et Biophysica Acta - Molecular Cell Research|
|Publication status||Published - 2008 May|
Bibliographical noteFunding Information:
This work was supported by the research grant from a Vascular System Research Center grant from KOSEF, Korea Research Foundation Grant funded by Korea Government (MOEHRD, basic Research Promotion Fund) (KRF-2005-204-C00051) (to M-K Bae), and MRC program of MOST/KOSEF (R13-2005-009) (to S-K Bae).
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology