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Int J Biol Sci 2018; 14(12):1696-1708. doi:10.7150/ijbs.27774

Research Paper

GLP-1 treatment protects endothelial cells from oxidative stress-induced autophagy and endothelial dysfunction

Xiangsheng Cai1,3, Miaoqin She2, Mingyu Xu3, Huiying Chen3, Jingjing Li3, Xinglu Chen1, Dianpeng Zheng3, Jun Liu4, Shangliang Chen5, Jianbin Zhu6, Xiaosong Xu1, Ruiying Li1, Jinlong Li3, Shaolian Chen1✉, Xiaorong Yang1✉, Hongwei Li3✉

1. Clinical Laboratory, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, People's Republic of China.
2. Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences. Guangzhou, 510660, People's Republic of China.
3. Institute of Biotherapy, Southern Medical University, Guangzhou, 510515, People's Republic of China.
4. Dermatology Hospital of Southern Medical University, Guangzhou, 510091, People's Republic of China.
5. ShenZhen Hospital, Southern Medical University, ShenZhen 518101, People's Republic of China.
6. Technology Center, Guangdong Vitalife Bio-tech Co.,LTD, FoShan, 528200, People's Republic of China.

Abstract

Endothelial dysfunction and excessively stimulated autophagy, often caused by oxidant injury or inflammation, will lead to atherosclerosis development and progression in diabetes. The aim of this study is to investigate the protective effect of glucagon-like peptide-1 (GLP-1) treatment on preventing oxidative stress-induced endothelial dysfunction and excessively stimulated autophagy. Treatment of endothelial cells with GLP-1 significantly attenuated oxidative stress-induced endothelial dysfunction and autophagy, which was associated with the reduction of intracellular reactive oxygen species (ROS) levels. These protective effects of GLP-1 were likely mediated by reducing phosphorylation of ERK1/2. We further demonstrated that GLP-1 treatment could reverse downregulation of epigenetic factor histone deacetylase 6 (HDAC6), a downstream molecular of the EKR1/2, induced by oxidant injury. In conclusion, our results suggest that GLP-1 produces a protective effect on endothelial cells from oxidant injury by preventing endothelial dysfunction and autophagy, which may be dependent on restoring HDAC6 through a GLP-1R-ERK1/2-dependent manner.

Keywords: oxidative stress, endothelial dysfunction, GLP-1, autophagy, HDAC6

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
How to cite this article:
Cai X, She M, Xu M, Chen H, Li J, Chen X, Zheng D, Liu J, Chen S, Zhu J, Xu X, Li R, Li J, Chen S, Yang X, Li H. GLP-1 treatment protects endothelial cells from oxidative stress-induced autophagy and endothelial dysfunction. Int J Biol Sci 2018; 14(12):1696-1708. doi:10.7150/ijbs.27774. Available from http://www.ijbs.com/v14p1696.htm