Published online before print August 11, 2005, doi: 10.1161/01.ATV.0000181744.58265.63
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© 2005 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Advanced Glycosylation End Products Might Promote Atherosclerosis Through Inducing the Immune Maturation of Dendritic Cells
From Shanghai Institute of Cardiovascular Disease (J.G., Q.J., Y.L., D.H., A.S., K.W., Y.Z., H.C.), Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China; and the Department of Cardiology (C.L.), Changzheng Hospital, the Second Military Medical University, Shanghai, People’s Republic of China.
Correspondence to Junbo Ge, MD, Professor of Medicine, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai 200032, P.R. China. E-mail gejunbo{at}zshospital.net
Objective— Both advanced glycosylation end products (AGEs) and dendritic cells (DCs) have been shown to play a causative role in atherosclerosis. However, whether they function interactively in the process remains uncertain. We therefore studied the effects of AGE–bovine serum albumin (AGE-BSA) on the maturation of DCs and the expressions of scavenger receptor-A (SR-A) and receptor for AGEs (RAGE) on DCs.
Methods and Results— AGE-BSA induced DCs maturation accompanied with increased expressions of CD1a, CD40, CD80, CD83, CD86, and MHC class II. The capacity of DCs to stimulate T-cell proliferation and secretion of cytokines (interferon [IFN], IFN-
, interleukin [IL]-10 and IL-12) was also enhanced by AGE-BSA. AGE-BSA significantly upregulated SR-A and RAGE expression on DCs and the upregulation was abolished by inhibition of mitogen-activated protein (MAP) kinase Jnk, but not by that of Erk and p38 MAP kinase. AGE-BSA–induced expression of CD83 and secretion of IL-12 were partly inhibited by either an anti-RAGE neutralizing antibody or a Jnk inhibitor.
Conclusions— AGE-BSA induces maturation of DCs and augmented their capacity to stimulate T-cell proliferation and cytokine secretions possibly through upregulation of RAGE and SR-A, which at least in part through Jnk. These findings might explain in part the interactive roles of AGEs and DCs in the processes of atherosclerosis.
We studied the effects of AGE-BSA on the maturation of DCs and the expressions of SR-A and RAGE on DCs. AGE-BSA–induced maturation of DCs and augmented their capacity to stimulate T-cell proliferation and cytokine secretions. These findings might explain in part the interactive roles of AGEs and DCs in the processes of atherosclerosis.
Key Words: advanced glycosylation end products • atherosclerosis • dendritic cells • immunity • receptor for advanced glycosylation end products
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