Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium. (2nd November 2015)

• Record Type: Journal Article
• Authors: Nam, Mi-Hyun; Son, Won-Rak; Lee, Young Sik; Lee, Kwang-Won
• Is Part Of: Cell communication & adhesion. Volume 22:Number 2/3/4/5/6(2015)
• Page Start: 67
• Page End: 78
• Publication Date: 2015-11-02
• Subjects: Advanced glycation end-products -- inflammatory cytokines -- reactive oxygen species -- vascular dysfunction; Cell adhesion -- Periodicals; Cell interaction -- Periodicals; Cellular signal transduction -- Periodicals; 571.6
• DOI: 10.1080/15419061.2016.1225196
• Languages: English
• ISSNs: 1541-9061

Abstract

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-α and interleukin-1β via extracellular-signal-regulated kinases phosphorylation and nuclear factor-κB 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.