Airborne particulate matter (PM2.5) triggers autophagy in human corneal epithelial cell line

被引:98
作者
Fu, Qiuli [1 ,2 ]
Lyu, Danni [1 ,2 ]
Zhang, Lifang [1 ,2 ]
Qin, Zhenwei [1 ,2 ]
Tang, Qiaomei [1 ,2 ]
Yin, Houfa [1 ,2 ]
Lou, Xiaoming [3 ]
Chen, Zhijian [3 ]
Yao, Ke [1 ,2 ]
机构
[1] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Eye Ctr, Hangzhou, Zhejiang, Peoples R China
[2] Zhejiang Prov Key Lab Ophthalmol, Hangzhou, Zhejiang, Peoples R China
[3] Zhejiang Prov Ctr Dis Control & Prevent, Dept Environm & Occupat Hlth, Hangzhou 310051, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
PM2.5; Autophagy; Human corneal epithelial cells; POLYCYCLIC AROMATIC-HYDROCARBONS; AIR-POLLUTION; OCULAR SURFACE; OXIDATIVE STRESS; INDUCED TOXICITY; AMBIENT LEVELS; LUNG INJURY; CHINA; CONJUNCTIVITIS; MECHANISMS;
D O I
10.1016/j.envpol.2017.04.078
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Purpose: To investigate particulate matter (PM2.5)-induced damage to human corneal epithelial cells (HCECs) and to determine the underlying mechanisms. Methods: HCECs were exposed to PM2.5 at a series of concentrations for various periods. Cell viability was measured by using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell proliferation was evaluated via 5-ethynyl-2'-deoxyuridine (EdU) analysis, while autophagy, was determined by immunofluorescence and Western blot. Results: PM2.5-induced cell damage of HCECs occurred in a time- and dose-dependent manner. Decreased cell viability and proliferation as well as increased apoptosis were observed in HCECs after PM2.5 exposure for 24 h. Autophagy in HCECs was slightly inhibited in the early stage (before 4 h) of exposure but significantly activated in the late stage (after 24 h), as evidenced by a decrease in the former and increase in the latter of the expression of the autophagy-associated markers LOB, ATG5, and BECN1. Interestingly, rapamycin, an autophagy activator, attenuated early-stage but aggravated late-stage PM2.5-induced cell damage, suggesting that the role of autophagy in HCECs may change over time during PM2.5 exposure. In addition, in the early stage, the expression of LOB and ATG5 increased in cells co-treated with rapamycin and PM2.5 compared to rapamycin-only or PM2.5-only treated cells, suggesting that autophagy may benefit cell viability after PM2.5 exposure. Conclusions: The results indicate the potential role of autophagy in the treatment of PM2.5-induced ocular corneal diseases and provide direct evidence for the cytotoxicity, possibly involving an autophagic process, of PM2.5 in HCECs. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:314 / 322
页数:9
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