Yu-Hong Cui1,2, Zi-Xuan Hu3, Zi-Xun Gao4, Xi-Ling Song3, Qing-Yang Feng5, Guang Yang3, Zhi-Jie Li4, Hong-Wei Pan3,4. 1. a Guangzhou Institute of Cardiovascular Disease , The Second Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University , Guangzhou , China. 2. b Department of Histology and Embryology, School of Basic Medical Sciences , Guangzhou Medical University , Guangzhou , China. 3. c Department of Public Health And Preventive Medicine, School of Medicine , Jinan University , Guangzhou , China. 4. d Institute of Ophthalmology, School of Medicine , Jinan University , Guangzhou , China. 5. e Department of Ophthalmology , Guangdong Women and Children's Hospital , Guangzhou , China.
Abstract
BACKGROUND: Cornea is the outmost structure of the eye and exposed directly to the air pollution. However, little is known about the effect of PM2.5 on corneal epithelium, which is critical for maintenance of cornea homeostasis and visual function. OBJECTIVE: We investigated the influence of PM2.5 exposure on corneal epithelial migration and the possible mechanisms involved in the process. METHODS: We observed wound healing in mouse model of cornea abrasion, evaluated the migration and mobility of cultured corneal epithelial cells with wound scratch assay and Transwell migration assay, detected the phosphorylation and interaction of FAK/paxillin with immunofluorescence and immunoprecipitation, and determined the RhoA activity and actin reorganization, in response to PM2.5 exposure. RESULTS: Exposure to PM2.5 remarkably inhibited corneal epithelial cell migration both in mouse model of corneal abrasion and in cell culture model. We found the phosphorylation and interaction of FAK/paxillin, RhoA activity as well as actin reorganization were suppressed by PM2.5 exposure. Moreover, formation of ROS might play a role in the action of PM2.5. CONCLUSIONS: PM2.5 exposure could result in delay of corneal epithelium wound healing by inhibiting cell migration, thus more attention should be paid to the potential risk of corneal infection and effort should be made to protect eyes against impairment induced by PM2.5.
BACKGROUND: Cornea is the outmost structure of the eye and exposed directly to the air pollution. However, little is known about the effect of PM2.5 on corneal epithelium, which is critical for maintenance of cornea homeostasis and visual function. OBJECTIVE: We investigated the influence of PM2.5 exposure on corneal epithelial migration and the possible mechanisms involved in the process. METHODS: We observed wound healing in mouse model of cornea abrasion, evaluated the migration and mobility of cultured corneal epithelial cells with wound scratch assay and Transwell migration assay, detected the phosphorylation and interaction of FAK/paxillin with immunofluorescence and immunoprecipitation, and determined the RhoA activity and actin reorganization, in response to PM2.5 exposure. RESULTS: Exposure to PM2.5 remarkably inhibited corneal epithelial cell migration both in mouse model of corneal abrasion and in cell culture model. We found the phosphorylation and interaction of FAK/paxillin, RhoA activity as well as actin reorganization were suppressed by PM2.5 exposure. Moreover, formation of ROS might play a role in the action of PM2.5. CONCLUSIONS: PM2.5 exposure could result in delay of corneal epithelium wound healing by inhibiting cell migration, thus more attention should be paid to the potential risk of corneal infection and effort should be made to protect eyes against impairment induced by PM2.5.