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

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

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243 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)886-895
Number of pages10
JournalBiochimica et Biophysica Acta - Molecular Cell Research
Issue number5
Publication statusPublished - 2008 May

Bibliographical note

Funding 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


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