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EGFR inhibitors regulate Ca2+ concentration and apoptosis after PM2.5 exposure based on a lung-mimic microfluidic system

文献类型： 外文期刊

作者： Zheng, Lulu 1 ; Wang, Yuwen 1 ; Zhang, Yule 1 ; Fu, Yongfeng 4 ; Yang, Zhijin 1 ; Fan, Yan 1 ; Sun, Zhen 5 ; Zhao, Manton 1 ;

作者机构： 1.Univ Shanghai Sci & Technol, Engn Res Ctr Opt Instrument & Syst, Shanghai Key Lab Modern Opt Syst, Minist Educ, 516 Jungong Rd, Shanghai 200093, Peoples R China

2.Fudan Univ, Dept Environm Sci & Engn, Shanghai Key Lab Atmospher Particle Pollut Preven, 220 Handan Rd, Shanghai 200433, Peoples R China

3.Tongji Univ, Shanghai Inst Intelligent Sci & Technol, Shanghai, Peoples R China

4.Fudan Univ, Sch Basic Med Sci, Dept Med Microbiol & Parasitol, Shanghai 200032, Peoples R China

5.Chinese Acad Fishery Sci, East China Sea Fisheries Res Inst, Shanghai 200090, Peoples R China

关键词： PM2.5; DNA methylation; Transcriptomic (RNA-Seq); Ca2+ concentration; Apoptosis

期刊名称：SCIENCE OF THE TOTAL ENVIRONMENT （ 影响因子：7.963； 五年影响因子：7.842 ）

ISSN： 0048-9697

年卷期： 2021 年 761 卷

页码：

收录情况： SCI

摘要： Air pollution has side effects on human health. Epidemiology studies indicate a positive association between ambient fine particle (PM2.5, or particles less than 2.5 mu m in diameter) concentration and lung cancer. However, how fine particles affect lung cancer at the molecular level and related therapeutic methods to address these diseases are unclear. Here, the multi-omics analysis (DNA methylation and transcriptomic) was used to detect human bronchial epithelial cells (HBE), that were exposed to PM2.5 using a quantified, small, portable, and organ-level air-liquid interface microfluidic system that mimics lung functions. The results indicate that 36,838 differentially methylated genes were detected. Of these 33,796 genes were hypomethylated (beta < 0), and 2862 genes were hypermethylated (beta > 0). RNA-Seq analysis demonstrated that 19,489 genes were upregulated (log(2)FC > 0), and 16,659 were downregulated. Furthermore, the calcium and apoptosis pathways were activated according to multi-omics analysis. The change in EGFR gene expression after PM2.5 exposure was the result of alterations of the cellular DNA methylome in the promoter. Inhibition or down-regulation of EGFR could result in the regulation of the downstream intracellular Ca2+ concentration and apoptosis via the EGFR/PLC gamma and EGFR/STAT/Bcl-XL pathways after PM2.5 exposure. EGFR inhibitors decrease the Ca2+ concentration of cells, thereby strengthening the effects of fine particles on apoptosis. In short, the Ca2+ concentration and the apoptosis of cells can be regulated via EGFR related pathway after PM2.5 exposure. The EGFR may be a potentially promising therapeutic target for the treatment of air pollution-induced lung cancer through regulation of the intracellular Ca2+ concentration and apoptosis. (C) 2020 Published by Elsevier B.V.

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