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PM2.5降尘诱导A549细胞G2/M期阻滞的机制研究
Mechanism of G2/M phase arrest in A549 cells induced by PM2.5 dust-fall
投稿时间:2017-08-30  修订日期:2017-10-30
中文关键词:PM2.5降尘  A549细胞  G2/M期阻滞  毒性机制
英文关键词:dust-fall (PM2.5)  A549 cell  G2/M phase arrest  cytotoxicity mechanism
基金项目:国家自然科学基金项目(41472046,41602033);四川省科技计划项目(2016JY0045)
作者单位E-mail
杨洁 西南医科大学, 四川 泸州 646000  
霍婷婷 西南科技大学 固体废物处理与资源化教育部重点实验室, 四川 绵阳 621010  
王玉琳 西南医科大学, 四川 泸州 646000  
董发勤 西南科技大学 固体废物处理与资源化教育部重点实验室, 四川 绵阳 621010  
曾娅莉 四川绵阳四○四医院, 四川 绵阳 621000  
邓建军 西南医科大学, 四川 泸州 646000;四川绵阳四○四医院, 四川 绵阳 621000 jianjundeng0801@163.com 
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中文摘要:
      PM2.5降尘作用于A549细胞后,MTT法检测细胞存活率,扫描电镜观察细胞形态,流式细胞术检测细胞周期改变,RT-PCR检测周期阻滞相关基因p53、p21、CDK1、c-myc和lncRNA H19的表达水平,Western-blot检测周期蛋白cyclin B1表达。通过转染H19 siRNA干扰H19的表达,RT-PCR检测其对p53、c-myc及CDK1表达的影响,以探讨PM2.5降尘诱导A549细胞周期阻滞的作用机制。结果显示,PM2.5降尘暴露可降低A549细胞存活率,随作用浓度及时间增加呈递减趋势,并可观察到细胞形态破坏,细胞膜表面吸附聚集大量粉尘颗粒。PM2.5作用于细胞24 h后,A549细胞增殖阻滞在G2/M期,周期阻滞相关基因p53、p21及H19表达增加,CDK1及cyclin B1表达降低。此外,转染H19 siRNA后成功干扰H19的表达,并调控CDK1表达进一步降低。综合以上结果,PM2.5降尘处理A549细胞后可通过激活p53及p21活性,抑制CDK1和cyclin B1表达水平,诱导G2/M期阻滞从而抑制细胞增殖。短期暴露于PM2.5后,lncRNA H19在染毒细胞中可能发挥特异性癌基因的作用,通过与p53及c-myc结合参与调控细胞周期,干扰H19低表达使细胞G2/M期阻滞更加明显。
英文摘要:
      In this study, A549 cells were exposed to PM2.5 dust-fall of different concentrations. MTT assay was used to evaluate cell viability. Cell morphology was observed through Scanning Electron Microscopy (SEM). Flow cytometry was used to detect the cell cycle induced by PM2.5. Then the expression levels of p53, p21, CDK1, c-myc and lncRNA H19 were detected by RT-PCR, and cyclin B1 was measured by Western-blot. In addition, the expression of p53, c-myc and CDK1 in A549 cell was detected after transferring H19 siRNA, with the purpose of investigating the mechanism of A549 cell cycle arrest induced by PM2.5. The results showed that, compared with the control group, A549 cell viability was declined in a dose-dependent manner and time-dependent effect. It was observed that cell morphology was changed and the cell membrane surface adsorbed a large amount of dust particles. The proliferation of A549 cells was inhibited in G2/M phase after being treated by PM2.5 for 24 h, and the expression of CDK1 and cyclin B1 was decreased by increasing the expression of p53, p21 and H19. In addition, the expression of H19 was successfully inhibited by transferring H19 siRNA, and then the expression of CDK1 was further decreased. It is inferred that exposure to PM2.5 could inhibit the expression of CDK1 and cyclin B1 by activating p53 and p21 activity, induce G2/M phase arrest, and finally inhibit A549 cell proliferation. In addition, after being exposed to PM2.5, lncRNA H19 may play a specific oncogenes role in treated cells in that it participated in the cell cycle progression by binding to p53 and c-myc, and hence low expression of H19 caused G2/M phase arrest more obviously.
杨洁,霍婷婷,王玉琳,董发勤,曾娅莉,邓建军,2017,PM2.5降尘诱导A549细胞G2/M期阻滞的机制研究[J].岩石矿物学杂志,36(6):894~902.
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