Zhou Zhixiang, Shao Tong, Qin Mengnan, Miao Xiaoyan, Chang Yu, Sheng Wang, Wu Fengshang, Yu Yunjiang
College of Life Science and Bioengineering, Beijing University of Technology, Beijing 100124, China.
College of Life Science and Bioengineering, Beijing University of Technology, Beijing 100124, China.
J Environ Sci (China). 2018 Apr;66:182-187. doi: 10.1016/j.jes.2017.05.019. Epub 2017 May 19.
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.
本研究的目的是检测从北京采集的PM2.5对人脐静脉内皮细胞（HUVEC）的直接毒性。细胞计数试剂盒8（CCK8）检测表明，暴露于PM2.5会以剂量依赖的方式降低HUVEC的增殖。我们还发现，暴露于PM2.5会诱导HUVEC自噬，证据如下：（1）双膜囊泡数量增加；（2）微管相关蛋白轻链3（LC3）的转化和点状化增强；（3）选择性自噬底物p62的水平随时间呈下降趋势。此外，用雷帕霉素促进暴露于PM2.5的HUVEC自噬可提高细胞存活率，而通过3-甲基腺嘌呤抑制自噬则显著降低细胞存活率。这些结果表明，暴露于PM2.5可诱导HUVEC的细胞毒性和自噬，且自噬对PM2.5诱导的细胞毒性起保护作用。本研究结果表明PM2.5对HUVEC有直接毒性作用，并为PM2.5暴露导致心血管疾病的机制提供了新的见解。
