Transcriptomic analyses of human bronchial epithelial cells BEAS-2B exposed to atmospheric fine particulate matter PM2.5
Transcriptomic analyses of human bronchial epithelial cells BEAS-2B exposed to atmospheric fine particulate matter PM2.5
复制标题
暴露于大气细颗粒物PM2.5的人支气管上皮细胞BEAS-2B的转录组分析
DOI：
10.1016/j.tiv.2017.04.014
复制
发表时间：
2017-08-01
影响因子：
3.2
通讯作者：
Sun, Zhiwei
中科院分区：
文献类型：
--
作者：
Li, Yang;Duan, Junchao;Sun, Zhiwei
呼吸道暴露是大气PM2.5进入人体的主要途径。流行病学研究表明，暴露于PM2.5与肺部疾病的风险增加有关，但其潜在机制仍不清楚。本研究以人支气管上皮细胞（BEAS-2B）为研究对象，采用基因芯片技术和生物信息学分析方法，研究了PM2. 5对BEAS-2B细胞的毒性效应和基因表达的影响。基因本体（GO）分析表明PM2.5引起了一系列重要功能相关基因表达模式的显著变化，包括基因转录、信号转导、细胞增殖、细胞代谢过程、免疫应答等。此外，通路分析和信号网络分析表明，PI 3 K/Akt、MAPK、和TNF信号通路是PM2.5影响最显著的信号通路，在调节细胞增殖、分化、细胞骨架调节和炎症反应等方面发挥重要作用。最后，为了验证基因芯片分析的准确性，从信号网络中筛选出上述信号通路中的部分关键基因，采用qRT-PCR检测其表达。我们的研究为PM2.5引起肺部疾病的分子机制提供了大量的信息，后续研究仍需进一步探索。
Respiratory exposure is the major route of atmospheric PM2.5 entering the human body. Epidemiological studies have indicated that exposure to PM2.5 is associated with increased risk of pulmonary diseases, but the underlying mechanisms remain less clear. In this study, human bronchial epithelial cells (BEAS-2B) were used to investigate the toxic effect and gene expression changes induced by PM2.5 collected from Beijing, China, based on microarray and following bioinformatic analyses. Gene ontology (GO) analysis indicated that PM2.5 caused significant changes in gene expression patterns related to a series of important functions, covering gene transcription, signal transduction, cell proliferation, cellular metabolic processes, immune response, etc. Additionally, pathway analysis and signal-net analysis showed that PI3K/Akt, MAPK, and TNF signaling pathways were the most prominently significant pathways affected by PM2.5, which play key roles in regulating cell proliferation, cell differentiation, cytoskeleton regulation, and inflammatory response. Finally, for the purpose of verifing the accuracy of microarray analysis, qRT-PCR was used to detect the expression of part key genes in the above signaling pathways, which were selected from the signal-net. Our study provided a large amount of information on the molecular mechanism that underling PM2.5 caused pulmonary diseases, and follow-up researches are still needed for further exploration.