摘要
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 dosedependent 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.
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 dosedependent 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.
基金
supported by the National Natural Science Foundation of China (Nos. 21677006, 21177119)
the State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences (No. SKLECRA2016OFP)
the State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences (No. KF2015-19)
