The effects of autophagy on vascular endothelial cells induced by airborne PM2.5
Zhixiang Zhou , Tong Shao , Mengnan Qin , Xiaoyan Miao , Yu Chang , Wang Sheng , Fengshang Wu , Yunjiang Yu
DOI:10.1016/j.jes.2017.05.019
Received January 24, 2017,Revised January 01, 1900, Accepted May 12, 2017, Available online May 19, 2017
Volume 30,2018,Pages 182-187
The purpose of this study was to examine the direct toxicity of PM2.5 collected from Beijing on human umbilical vein endothelial cells (HUVEC). A Cell Counting Kit 8 (CCK8) assay demonstrated that PM2.5 exposure decreased the proliferation of HUVECs in a dose-dependent manner. We also found that PM2.5 exposure induced autophagy in HUVECs, as evidenced by: (1) an increased number of double-membrane vesicles; (2) enhanced conversion and punctuation of the microtubule-associated protein light chain 3 (LC3); and (3) decreased levels of the selective autophagy substrate p62 in a time-dependent manner. Furthermore, promoting autophagy in PM2.5-exposed HUVECs with rapamycin increased the cell survival rate, whereas inhibiting autophagy via 3-methyladenine significantly decreased cell survival. These results demonstrate that PM2.5 exposure can induce cytotoxicity and autophagy in HUVECs and that autophagy play a protective role against PM2.5-induced cytotoxicity. The findings of the present study imply a direct toxic effect of PM2.5 on HUVECs and provide novel insight into the mechanism of cardiovascular diseases caused by PM2.5 exposure.
