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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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-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
Volume1783
Issue number5
DOIs
Publication statusPublished - 2008 May 1

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Nicotinamide Phosphoribosyltransferase
Vascular Cell Adhesion Molecule-1
Intercellular Adhesion Molecule-1
Endothelial Cells
Blood Vessels
Adipokines
Cell Adhesion Molecules
Vascular Diseases
Endothelium
Leukocytes
Obesity
Phosphorylation
Inflammation

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Cite this

Kim, Su Ryun ; Bae, Yun Hee ; Bae, Soo Kyung ; Choi, Kyu Sil ; Yoon, Kwon Ha ; Koo, Tae Hyeon ; Jang, Hye Ock ; Yun, Il ; Kim, Kyu Won ; Kwon, Young Guen ; Yoo, Mi Ae ; Bae, Moon Kyoung. / Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-κB activation in endothelial cells. In: Biochimica et Biophysica Acta - Molecular Cell Research. 2008 ; Vol. 1783, No. 5. pp. 886-895.
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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-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.",
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Kim, SR, Bae, YH, Bae, SK, Choi, KS, Yoon, KH, Koo, TH, Jang, HO, Yun, I, Kim, KW, Kwon, YG, Yoo, MA & Bae, MK 2008, 'Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-κB activation in endothelial cells', Biochimica et Biophysica Acta - Molecular Cell Research, vol. 1783, no. 5, pp. 886-895. https://doi.org/10.1016/j.bbamcr.2008.01.004

Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-κB activation in endothelial cells. / Kim, Su Ryun; Bae, Yun Hee; Bae, Soo Kyung; Choi, Kyu Sil; Yoon, Kwon Ha; Koo, Tae Hyeon; Jang, Hye Ock; Yun, Il; Kim, Kyu Won; Kwon, Young Guen; Yoo, Mi Ae; Bae, Moon Kyoung.

In: Biochimica et Biophysica Acta - Molecular Cell Research, Vol. 1783, No. 5, 01.05.2008, p. 886-895.

Research output: Contribution to journalArticle

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T1 - Visfatin enhances ICAM-1 and VCAM-1 expression through ROS-dependent NF-κB activation in endothelial cells

AU - Kim, Su Ryun

AU - Bae, Yun Hee

AU - Bae, Soo Kyung

AU - Choi, Kyu Sil

AU - Yoon, Kwon Ha

AU - Koo, Tae Hyeon

AU - Jang, Hye Ock

AU - Yun, Il

AU - Kim, Kyu Won

AU - Kwon, Young Guen

AU - Yoo, Mi Ae

AU - Bae, Moon Kyoung

PY - 2008/5/1

Y1 - 2008/5/1

N2 - 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.

AB - 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.

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