GLP-1 treatment protects endothelial cells from oxidative stress-induced autophagy and endothelial dysfunction
| Autor: | Xiangsheng Cai, Dianpeng Zheng, Shangliang Chen, She Miaoqin, Xu Xiaosong, Jingjing Li, Yang Xiaorong, Jianbin Zhu, Jinlong Li, Chen Shaolian, Huiying Chen, Xinglu Chen, Hongwei Li, Ruiying Li, Liu Jun, Mingyu Xu |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
endocrine system autophagy Inflammation Oxidative phosphorylation medicine.disease_cause Histone Deacetylase 6 Applied Microbiology and Biotechnology endothelial dysfunction Glucagon-Like Peptide-1 Receptor 03 medical and health sciences Downregulation and upregulation Glucagon-Like Peptide 1 Human Umbilical Vein Endothelial Cells Medicine Humans Endothelial dysfunction Molecular Biology Ecology Evolution Behavior and Systematics Membrane Potential Mitochondrial business.industry Autophagy Endothelial Cells Cell Biology HDAC6 medicine.disease Peptide Fragments Oxidative Stress 030104 developmental biology Cancer research Phosphorylation medicine.symptom business GLP-1 Reactive Oxygen Species Oxidative stress Developmental Biology Research Paper |
| Zdroj: | International Journal of Biological Sciences |
| ISSN: | 1449-2288 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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