Xiaojie Ding1, Meilin Wang1, Haiyan Chu1, Minjie Chu2, Tong Na3, Yang Wen2, Dongmei Wu1, Bin Han4, Zhipeng Bai4, Weihong Chen5, Jing Yuan5, Tangchun Wu5, Zhibin Hu2, Zhengdong Zhang6, Hongbing Shen7. 1. Department of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, China; Department of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China. 2. Department of Epidemiology and Biostatistics, School of Public Health, Nanjing Medical University, Nanjing, China. 3. Department of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, China. 4. State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing, China. 5. China Key Laboratory for Environment and Health of Ministry of Education, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. 6. Department of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, China; Department of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China. Electronic address: drzdzhang@gmail.com. 7. Department of Epidemiology and Biostatistics, School of Public Health, Nanjing Medical University, Nanjing, China. Electronic address: hbshen@njmu.edu.cn.
Abstract
BACKGROUND: Many studies have linked ambient fine particulate matter (PM2.5) air pollution to different cardiopulmonary diseases in the general population. However the complex mechanisms underlying PM2.5-induced adverse health effects are not yet to be fully elucidated. METHOD: In this study, we aimed to identify genes and pathways that may contribute to PM2.5-induced lung toxicity in humans through genome-wide approaches. Human bronchial epithelial (HBE) cells, exposed to various concentrations of PM2.5 collected from Wuhan, China, showed decreased cell viability in a dose-dependent manner. HBE cells were exposed to 200 μg/ml and 500 μg/ml PM2.5 and microarrays were used to obtain a global view of the transcriptomic responses. RESULTS: A total of 970 and 492 genes were identified that significantly changed after 200 μg/ml and 500 μg/ml PM2.5 exposures, respectively. PM2.5 induced a large number of genes involved in inflammatory and immune response, response to oxidative stress, and response to DNA damage stimulus, which might contribute to PM2.5 related cardiopulmonary diseases. Pathway analysis revealed that different dose of PM2.5 triggered partially common disturbed pathways. Flow cytometry assay evidenced that there were statistically significant differences in the G1 phase of cell cycle after low or high-dose PM2.5 exposure when compared to the unexposed controls. Only high-dose PM2.5 significantly increased the proportion of cells in the S phase of cell cycle. CONCLUSION: We identified many genes and pathways that altered significantly in HBE cells after PM2.5 exposures. These findings are important in providing further understanding of the mechanisms underlying PM2.5-induced adverse health effects.
BACKGROUND: Many studies have linked ambient fine particulate matter (PM2.5) air pollution to different cardiopulmonary diseases in the general population. However the complex mechanisms underlying PM2.5-induced adverse health effects are not yet to be fully elucidated. METHOD: In this study, we aimed to identify genes and pathways that may contribute to PM2.5-induced lung toxicity in humans through genome-wide approaches. Human bronchial epithelial (HBE) cells, exposed to various concentrations of PM2.5 collected from Wuhan, China, showed decreased cell viability in a dose-dependent manner. HBE cells were exposed to 200 μg/ml and 500 μg/ml PM2.5 and microarrays were used to obtain a global view of the transcriptomic responses. RESULTS: A total of 970 and 492 genes were identified that significantly changed after 200 μg/ml and 500 μg/ml PM2.5 exposures, respectively. PM2.5 induced a large number of genes involved in inflammatory and immune response, response to oxidative stress, and response to DNA damage stimulus, which might contribute to PM2.5 related cardiopulmonary diseases. Pathway analysis revealed that different dose of PM2.5 triggered partially common disturbed pathways. Flow cytometry assay evidenced that there were statistically significant differences in the G1 phase of cell cycle after low or high-dose PM2.5 exposure when compared to the unexposed controls. Only high-dose PM2.5 significantly increased the proportion of cells in the S phase of cell cycle. CONCLUSION: We identified many genes and pathways that altered significantly in HBE cells after PM2.5 exposures. These findings are important in providing further understanding of the mechanisms underlying PM2.5-induced adverse health effects.
Authors: Shi Xi Chen; Xiao Zhen Yang; Ying Deng; Jing Huang; Yan Li; Qian Sun; Chang-Ping Yu; Yong Zhu; Wan Shu Hong Journal: Chemosphere Date: 2016-12-07 Impact factor: 7.086
Authors: Kamaljeet Kaur; Isabel C Jaramillo; Raziye Mohammadpour; Anne Sturrock; Hamidreza Ghandehari; Christopher Reilly; Robert Paine; Kerry E Kelly Journal: J Environ Sci Health A Tox Hazard Subst Environ Eng Date: 2019-07-25 Impact factor: 2.269
Authors: Sandra V Pirela; Georgios A Sotiriou; Dhimiter Bello; Martin Shafer; Kristin Lee Bunker; Vincent Castranova; Treye Thomas; Philip Demokritou Journal: Nanotoxicology Date: 2014-11-11 Impact factor: 5.913
Authors: Michelle C Turner; Zorana J Andersen; Andrea Baccarelli; W Ryan Diver; Susan M Gapstur; C Arden Pope; Diddier Prada; Jonathan Samet; George Thurston; Aaron Cohen Journal: CA Cancer J Clin Date: 2020-08-25 Impact factor: 508.702
Authors: Pek Xyen Tan; Krishnapriya Thiyagarasaiyar; Cheng-Yau Tan; You-Jin Jeon; Mohd Shahrul Mohd Nadzir; Yong-Jiang Wu; Liang-Ee Low; Atanas G Atanasov; Long Chiau Ming; Kai Bin Liew; Bey-Hing Goh; Yoon-Yen Yow Journal: Mar Drugs Date: 2021-05-30 Impact factor: 5.118