Epidermal growth factor protects against ultraviolet damage in human corneal epithelial cells through inhibiting autophagy

被引:0
作者
Huo, Yanan [1 ]
Jiang, Bo [2 ]
Zheng, Xiaoxiao [3 ]
Chen, Wei [3 ]
Xie, Xin [1 ]
机构
[1] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Ctr Eye, 88 Jiefang Rd, Hangzhou 310009, Zhejiang, Peoples R China
[2] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Dept Ophthalmol, Hangzhou 310003, Zhejiang, Peoples R China
[3] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Surg, Hangzhou, Zhejiang, Peoples R China
基金
浙江省自然科学基金; 中国国家自然科学基金;
关键词
Epidermal growth factor; ultraviolet radiation; autophagy; reactive oxygen species; OXIDATIVE-STRESS; INDUCED APOPTOSIS; SKIN;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Damage of human corneal epithelial cells is often induced by exposure to various kinds of light including sunlight and artificial light. To determine the cytoprotective effects and the underlying mechanisms of epidermal growth factor (EGF) in human corneal epithelial (HCE) cells exposed to ultraviolet (UV) radiation. We found that cell viability as measured by CCK-8 assay and EDU incorporation assay was significantly decreased in HCE cells after UV exposure, while treatment with EGF promoted cell proliferation. EGF decreased the levels of LC3-I and LC3-II, the number of autophagosomes and autophagolysosomes in HCE cells exposed UV radiation. When cell autophagy was blocked by chloroquine, the cytoprotective effect of EGF was diminished as determined by cell viability assay. Furthermore, when HCE cells were treated with the ROS inhibitor NAC, cell viability was significantly decreased in EGF treated group compared with UV radiation only. In conclusion, these findings indicate that EGF has protective role in UV radiation induced HCE cell damage by inhibiting autophagy which might be mediated by increasing the production of ROS.
引用
收藏
页码:9008 / 9017
页数:10
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