The role of autophagy in advanced glycation end product-induced proliferation and migration in rat vascular smooth muscle cells | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 13، دوره 21، شماره 6، شهریور 2018، صفحه 634-638 اصل مقاله (939.1 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2018.20266.5305 | ||
| نویسندگان | ||
| Zhigang Liu1؛ Shuwei Huang2؛ Pengfei Hu2؛ Hui Zhou* 3 | ||
| 1Department of Cardiology, Yidu Central Hospital of Weifang, Qingzhou, Shandong, 262500, China | ||
| 2Department of Cardiology, Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China | ||
| 3Department of Cardiology, Zhejiang hospital, Hangzhou, 310013), China | ||
| چکیده | ||
| Objective(s): To investigate the role of autophagy in advanced glycation end products (AGEs)-induced proliferation and migration in rat vascular smooth muscle cells (VSMCs). Materials and Methods: After culture, VSMCs were treated with 0, 1, 10, and 100 μg/ml concentrations of AGEs. Autophagy specific protein light chain 3 (LC3)-I/II was determined by western blotting, autophagosomes were observed with electron microscopy, cell proliferation was quantified using the methyl thiazolyl tetrazolium (MTT) assay, and cell migration was evaluated using Transwell migration and scratch assays. Results: Compared to the control group, the level of LC3- II/I in AGEs treatment group was up-regulated, and the number of autophagosomes was also increased. Furthermore, in concentration of 100 μg/ml AGEs, the extent of proliferation and migration was significantly increased compared to the control group. However, pretreating cells with autophagy inhibitor 3-MA could attenuate these effects. Conclusion: Our study demonstrated that AGEs-induced autophagy accelerated AGEs-stimulated proliferation and migration in VSMCs. | ||
| کلیدواژهها | ||
| Advanced Glycation End Products؛ Autophagy؛ Cell Proliferation؛ Muscle؛ Smooth؛ Transcellular cell migration؛ Vascular | ||
| مراجع | ||
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