Abstract
The glyoxal-lysine dimer (GOLD), which is a glyoxal (GO)-derived advanced glycation end product (AGE), is produced by the glycation reaction. In this study, we evaluated the effect of GOLD on the oxidative damage and inflammatory response in SV40 MES 13 mesangial cells. GOLD significantly increased the linkage with the V-type immunoglobulin domain of RAGE, a specific receptor of AGE. We found that GOLD treatment increased RAGE expression and reactive oxygen species (ROS) production in mesangial cells. GOLD remarkably regulated the protein and mRNA expression of nuclear factor erythroid 2-related factor 2 (NRF2) and glyoxalase 1 (GLO1). In addition, mitochondrial deterioration and inflammation occurred via GOLD-induced oxidative stress in mesangial cells. GOLD regulated the mitogen-activated protein kinase (MAPK) and the release of proinflammatory cytokines associated with the inflammatory mechanism of mesangial cells. Furthermore, oxidative stress and inflammatory responses triggered by GOLD were suppressed through RAGE inhibition using RAGE siRNA. These results demonstrate that the interaction of GOLD and RAGE plays an important role in the function of mesangial cells.
Highlights
Advanced glycation end products (AGEs) are stable proteins with post-translational modifications formed through spontaneous reactions with glucose and metabolite such as glyoxal and methylglyoxal
We confirmed that the protein and mRNA levels of receptor for AGEs (RAGE) increased with AGE production (Figure 1C,D)
This study identified a specific mechanism through the effect that glyoxal-lysine dimer (GOLD), a GO-inThis study identified a specific mechanism through the effect that GOLD, a GOduced AGE produced by glycation, produces excessive reactive oxygen species (ROS) production and induces an induced AGE produced by glycation, produces excessive ROS production and induces inflammatory response in mesangial cells
Summary
Advanced glycation end products (AGEs) are stable proteins with post-translational modifications formed through spontaneous reactions with glucose and metabolite such as glyoxal and methylglyoxal. They are a large, heterogeneous group of compounds resulting from nonenzymatic Maillard reactions between reducing sugars and proteins, lipids, or nucleic acids, which can be produced both in vitro and in vivo [1,2]. The effect of AGE consumption on the development of chronic diseases has remained inconclusive. Previous studies have shown the effect of an inflammatory response and oxidative stress after AGE consumption between healthy and diseased conditions. AGEs have a significant impact on the development and development of kidney damage
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