Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium
- Authors
- Nam, Mi-Hyun; Son, Won-Rak; Lee, Young Sik; Lee, Kwang-Won
- Issue Date
- 2015
- Publisher
- TAYLOR & FRANCIS INC
- Keywords
- Advanced glycation end-products; inflammatory cytokines; reactive oxygen species; vascular dysfunction
- Citation
- CELL COMMUNICATION AND ADHESION, v.22, no.2-6, pp.67 - 78
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELL COMMUNICATION AND ADHESION
- Volume
- 22
- Number
- 2-6
- Start Page
- 67
- End Page
- 78
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/96220
- DOI
- 10.1080/15419061.2016.1225196
- ISSN
- 1541-9061
- Abstract
- Advanced glycation end-products (AGEs) are involved in the development of vascular smooth muscle cell (VSMC) dysfunction and the progression of atherosclerosis. However, AGEs may indirectly affect VSMCs via AGEs-induced signal transduction between monocytes and human umbilical endothelial cells (HUVECs), rather than having a direct influence. This study was designed to elucidate the signaling pathway underlying AGEs-RAGE axis influence on VSMC dysfunction using a co-culture system with monocytes, HUVECs and VSMCs. AGEs stimulated production of reactive oxygen species and pro-inflammatory mediators such as tumor necrosis factor-a and interleukin-1 beta via extracellular-signal-regulated kinases phosphorylation and nuclear factor-jB activation in HUVECs. It was observed that AGEs-induced pro-inflammatory cytokines increase VSMC proliferation, inflammation and vascular remodeling in the co-culture system. This result implies that RAGE plays a role in AGEs-induced VSMC dysfunction. We suggest that the regulation of signal transduction via the AGEs-RAGE axis in the endothelium can be a therapeutic target for preventing atherosclerosis.
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Collections - College of Life Sciences and Biotechnology > Division of Biotechnology > 1. Journal Articles
- Graduate School > Department of Biotechnology > 1. Journal Articles
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