Advanced glycation end products inhibit glucose-6-phosphate dehydrogenase activity and expression in human umbilical vein endothelial cells.
- Author:
Mei-Hua HE
1
;
Yan ZHANG
Author Information
1. Department of Anatomy, School of Basic Medical Sciences, Peking University, Beijing 100191, China. hemeihua@bjmu.edu.cn
- Publication Type:Journal Article
- MeSH:
Antioxidants;
metabolism;
Cells, Cultured;
Glucosephosphate Dehydrogenase;
antagonists & inhibitors;
metabolism;
Glycation End Products, Advanced;
pharmacology;
Human Umbilical Vein Endothelial Cells;
drug effects;
enzymology;
Humans;
Oxidative Stress;
Reactive Oxygen Species;
metabolism;
Serum Albumin, Bovine;
pharmacology
- From:
Acta Physiologica Sinica
2012;64(6):646-650
- CountryChina
- Language:English
-
Abstract:
Increased formation of advanced glycation end-products (AGEs) is occurred in hyperglyceamia and diabetes, leading to oxidative stress and progression of diabetic vascular diseases. Glucose-6-phosphate dehydrogenase (G6PD), the principal source of NADPH, serves as an antioxidant enzyme to modulate the redox milieu. Deficiency of G6PD activity is associated with increased endothelial cell oxidative stress. Current study is designed to investigate the effects of AGEs on G6PD activity and expression in human umbilical vein endothelial cells. Treatment of AGE-modified bovine serum albumin (AGE-BSA, 100 µg/mL, 24 h), but not native BSA, to human umbilical vein endothelial cells increased ROS generation by (48.89 ± 5.28)%. G6PD activity was decreased by AGE-BSA treatment by (61.25 ± 11.2)%. The expression of G6PD at mRNA and protein levels was also decreased by AGE-BSA treatment by (27.92 ± 6.73)% and (23.72 ± 2.44)%, respectively. These results suggest that AGEs could result in G6PD deficiency in human umbilical vein endothelial cells by inhibiting the expression of G6PD at mRNA and protein levels and G6PD activity.
