Journal
ATHEROSCLEROSIS
Volume 208, Issue 1, Pages 34-42Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2009.06.007
Keywords
Advanced glycation end products; Receptor for advanced glycation end products; Adventitial fibroblasts; Cell movement; Inflammatory response; Mitogen activated protein kinase; Angiotensin receptor blocker
Funding
- Major National Basic Research Development Program of the People's Republic of China [2005CB523309]
- Science & Technology Commission of Shanghai Municipality [08JC1407300]
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Objective: Advanced glycation end products (AGEs) and vascular adventitial fibroblasts (AFs) are involved in diabetes-related vascular complications. However, the effect of AGEs on AFs remains unclear. The aim of this study was to observe the impact of AGEs on cell migration capacity and associated inflammatory responses of AFs. Methods and results: Isolated vascular AFs of Sprague-Dawley rats were cultured, harvested after 24 h synchronization and challenged with AGE-HSA. AGE-HSA upregulated the expression of receptor for advanced glycation end products (RAGE), significantly increased the migration capacity and inflammatory mediators MCP-1, IL-6, VCAM-1 expressions on AFs. These effects could be significantly attenuated by anti-RAGE neutralizing antibody, p38, ERK1/2 and JNK MAPK inhibitors as well as by candesartan. AGE-HAS also upregulated NF-kappa B transcriptional activity and I-kappa B-alpha phosphorylation, effect that was significantly inhibited by candesartan. Conclusions: AGE-HSA increased the migration capacity and inflammatory responses of rat AFs via RAGE-MAPK-NF-kappa B pathways. Candesartan effectively inhibited these effects which might be a novel vascular protection mechanism of candesartan. (C) 2009 Published by Elsevier Ireland Ltd.
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