张国艳, 雷立健, 张真, 郭建勇, 康辉. 微小RNA-21在镉染毒HEK293细胞中的表达[J]. 环境与职业医学, 2017, 34(5): 436-440. DOI: 10.13213/j.cnki.jeom.2017.16730
引用本文: 张国艳, 雷立健, 张真, 郭建勇, 康辉. 微小RNA-21在镉染毒HEK293细胞中的表达[J]. 环境与职业医学, 2017, 34(5): 436-440. DOI: 10.13213/j.cnki.jeom.2017.16730
ZHANG Guo-yan, LEI Li-jian, ZHANG Zhen, GUO Jian-yong, KANG Hui. Expression of microRNA-21 induced by cadmium exposure in HEK293 cells[J]. Journal of Environmental and Occupational Medicine, 2017, 34(5): 436-440. DOI: 10.13213/j.cnki.jeom.2017.16730
Citation: ZHANG Guo-yan, LEI Li-jian, ZHANG Zhen, GUO Jian-yong, KANG Hui. Expression of microRNA-21 induced by cadmium exposure in HEK293 cells[J]. Journal of Environmental and Occupational Medicine, 2017, 34(5): 436-440. DOI: 10.13213/j.cnki.jeom.2017.16730

微小RNA-21在镉染毒HEK293细胞中的表达

Expression of microRNA-21 induced by cadmium exposure in HEK293 cells

  • 摘要: 目的 探讨不同浓度镉致人胚胎肾细胞(HEK293细胞)中微小RNA(miRNA)-21(miR-21)表达的改变。

    方法 培养HEK293细胞,细胞经0、30、60、120 μmol/L CdCl2染毒1、3、6、12 h后,MTT法测定细胞生长情况,qRT-PCR检测miR-21表达量。

    结果 随着CdCl2浓度的增高,作用时间的延长,细胞的生长受到抑制。在CdCl2浓度为120 μmol/L,染毒时间为12 h时抑制率达到最大,此时细胞生存率为8.57%。当作用时间分别为1、3、6、12 h时,不同浓度CdCl2染毒的细胞中miR-21的表达量差别有统计学意义(均P < 0.01),且miR-21的表达量随着CdCl2染毒浓度的增加而增加(均Ptrend < 0.01);当CdCl2浓度分别为30、60、120 μmol/L时,作用不同时间,细胞中miR-21表达量差别也有统计学意义(均P < 0.05);在CdCl2浓度为30 μmol/L和120 μmol/L时,miR-21表达量随CdCl2作用时间的延长而增高(Ptrend=0.030,Ptrend=0.011);在CdCl2浓度为120μmol/L且染毒时间为12 h时,miR-21表达量最大,为27.77。

    结论 镉染毒可导致HEK293细胞miR-21表达上调。

     

    Abstract: Objective To test the effects on the expression of microRNA(miRNA)-21 (miR-21) in human embryonic kidney cells (HEK293 cells) induced by cadmium.

    Methods HEK293 cells were cultured with 0, 30, 60, and 120 μmol/L of cadmium chloride (CdCl2) for 1, 3, 6 and 12 h, respectively. MTT was used to test cell growth. The miR-21 expression was detected by qRT-PCR.

    Results With the increasing of CdCl2 concentrations and action time, the inhibition to cells growth was observed. The inhibition rate reached maximum after 12 h treatment at 120 μmol/L CdCl2, and the corresponding viability was 8.57%. At the same exposure time, differences in the expression of miR-21 were observed among cells treated with different concentrations of CdCl2 (P < 0.01), and the expression of miR-21 was up-regulated with increasing concentrations of CdCl2 (Ptrend < 0.01). At the same concentration of CdCl2, different action time of CdCl2 resulted in different expressions of miR-21 (P < 0.05). With action time extending, the expression of miR-21 was up-regulated at 30 μmol/L and 120 μmol/L CdCl2 (Ptrend=0.030, Ptrend=0.011). The expression of miR-21 reached maximum after treatment with 120μmol/L CdCl2 for 12 h, and the relative expression of miR-21 was 27.77.

    Conclusion Cadmium exposure could up-regulate the expression of miR-21.

     

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