Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:645-651
© 2000 American Heart Association, Inc.
Vascular Biology |
Angiotensin II Stimulates Endothelial Vascular Cell Adhesion Molecule-1 via Nuclear Factor-
B Activation Induced by Intracellular Oxidative Stress
From INSERM U460 (M.E.P., W.G., F.S., J.-B.M.) and INSERM U430 (A.N.), Paris, and INSERM U397 (J.-F.A.), Toulouse, France.
Correspondence to Dr Maria E. Pueyo, INSERM U460, Faculté de Médecine Xavier Bichat, 16, rue Henri Huchard, 75018 Paris, France. E-mail pueyo{at}infobiogen.fr
Abstract—The recruitment of
monocytes via the endothelial expression of vascular
cell adhesion molecule-1 (VCAM-1) is a key step in the formation of the
initial lesion in atherosclerosis. Because
angiotensin (Ang) II may be involved in this process, we
investigated its role on the signaling cascade leading to VCAM-1
expression in endothelial cells. Ang II stimulates mRNA
and protein expression of VCAM-1 in these cells via the AT1
receptor. This effect was enhanced by
NG-nitro-L-arginine methyl
ester, a nitric oxide synthase inhibitor, and blocked by
pyrrolidinedithiocarbamate, an antioxidant molecule. Ang II
activated the redox-sensitive transcription factor nuclear
factor-
B and stimulated the degradation of both inhibitor of B
(IB)
and IBß with different kinetics. The degradation of
IBs induced by Ang II was not modified by incubation with exogenous
superoxide dismutase and catalase, suggesting that this effect was not
mediated by the extracellular production of
O2-. In contrast, rotenone and antimycin, 2
inhibitors of the mitochondrial respiratory chain,
inhibited the Ang II–induced IB degradation, showing that
generation of reactive oxygen species in the mitochondria is involved
on Ang II action. BXT-51702, a glutathione peroxidase mimic, inhibited
the effect of Ang II, and aminotriazole, an inhibitor of
catalase, enhanced it, suggesting a role for
H2O2 in IB degradation. This is confirmed by
experiments showing that Ang II stimulates the intracellular
production of H2O2 in
endothelial cells. These results demonstrate that Ang
II induced an intracellular oxidative stress in
endothelial cells, which stimulates IB degradation
and nuclear factor-B activation. This activation enhances the
expression of VCAM-1 and probably other genes involved in the
early stages of atherosclerosis.
Key Words: endothelium • nuclear factor-B • IB • superoxide anions • hydrogen peroxide
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