To the Editor：Autophagy is reported to play a critical role in low shear stress （LSS）-induced endothelial cell injury and the formation of atherosclerotic plaques.[1] However,the corresponding mechanisms remain unc...To the Editor：Autophagy is reported to play a critical role in low shear stress （LSS）-induced endothelial cell injury and the formation of atherosclerotic plaques.[1] However,the corresponding mechanisms remain unclear.[2-8] This study was to investigate the changes and mechanism of LSS-induced autophagy in human umbilical vein endothelial cells （HUVECs）.HUVECs were treated with LSS of 5 dyn/cm2 for 0,5,15,30,and 60 min in a parallel plate flow chamber system.Light chain （LC） Ⅱ,LC3 Ⅰ,and p62,p38 mitogen-activated protein kinase （MAPK） and their protein of phosphorylation of p38 （p-p38） were detected with Western blot analysis.The protein levels of p-p53 （ser15） and their distribution were detected by immunofluorescence （IF）.展开更多
基金This study was supported by grants from the Natural Science Foundation of Guangdong Province （No. 2016A030313430）, the Scientific and Technological Program of Guangzhou City （No. 201510010024）, and the Natural Science Foundation of Guangdong Province （No. 2014A030310049）.
文摘To the Editor：Autophagy is reported to play a critical role in low shear stress （LSS）-induced endothelial cell injury and the formation of atherosclerotic plaques.[1] However,the corresponding mechanisms remain unclear.[2-8] This study was to investigate the changes and mechanism of LSS-induced autophagy in human umbilical vein endothelial cells （HUVECs）.HUVECs were treated with LSS of 5 dyn/cm2 for 0,5,15,30,and 60 min in a parallel plate flow chamber system.Light chain （LC） Ⅱ,LC3 Ⅰ,and p62,p38 mitogen-activated protein kinase （MAPK） and their protein of phosphorylation of p38 （p-p38） were detected with Western blot analysis.The protein levels of p-p53 （ser15） and their distribution were detected by immunofluorescence （IF）.
