文章摘要
张晓倩,张 昕,李 楠,池 霞,郭锡熔,童梅玲.miR-182在多氯联苯(PCB1254)暴露后视网膜神经节细胞内的表达及意义[J].南京医科大学学报,2017,(1):35~39
miR-182在多氯联苯(PCB1254)暴露后视网膜神经节细胞内的表达及意义
Expression and effects of miR-182 in retinal ganglion cells exposed to PCB1254
投稿时间:2016-05-30  
DOI:10.7655/NYDXBNS20170107
中文关键词: 多氯联苯  PCB1254  miR-182  RGC-5细胞  细胞增殖  细胞凋亡
英文关键词: polychlorinated biphenyls  PCB1254  miR-182  RGC-5  cell apoptosis  cell proliferation
基金项目:国家自然科学基金(81170889);江苏省“六大人才高峰”第七批高层次人才项目(2010001);南京市医学科技发展基金项目(YKK10032)
作者单位
张晓倩 南京医科大学儿科研究所江苏 南京 210029南京市中医院儿科江苏 南京 210001 
张 昕 南京医科大学附属妇产医院儿童保健科江苏 南京 210004 
李 楠 南京医科大学儿科研究所江苏 南京 210029 
池 霞 南京医科大学儿科研究所江苏 南京 210029
南京医科大学附属妇产医院儿童保健科江苏 南京 210004 
郭锡熔 南京医科大学儿科研究所江苏 南京 210029
南京医科大学附属妇产医院儿童保健科江苏 南京 210004 
童梅玲 南京医科大学附属妇产医院儿童保健科江苏 南京 210004 
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中文摘要:
      目的:研究多氯联苯(polychlorinated biphenyls,PCBs)PCB1254引起视网膜神经节细胞毒性作用的可能机制。方法:分别配制浓度为0.125、0.250、0.500、1.000 mg/L的PCB1254对RGC-5细胞进行暴露处理,并设立空白对照及0.01%甲醇对照组,测定细胞内miR-182表达水平;利用miR-182类似物或抑制剂转染RGC-5细胞,使miR-182上调或下调,分别检测细胞凋亡、细胞增殖功能和细胞周期;使用0.5、1.0 mg/L的PCB1254刺激RGC-5细胞,再转染miR-182类似物,分别检测细胞凋亡、细胞增殖功能。结果:随着PCB1254浓度的增高,RGC-5细胞内miR-182的表达逐渐被抑制,当浓度≥0.5 mg/L时,与对照组的差异有统计学意义(P<0.05)。在RGC-5细胞内沉默miR-182可导致Caspase-3活性增高(P<0.05),表明miR-182沉默促进细胞凋亡;CCK-8法显示miR-182沉默会导致RGC-5细胞活力降低(P<0.05),表明miR-182沉默会抑制细胞增殖;MiR-182沉默对RGC-5细胞周期无显著影响(P>0.05)。使用miR-182 类似物干预0.5、1.0 mg/L PCB1254暴露后的RGC-5细胞,发现细胞内 Caspase-3活性下降(P<0.05)、细胞活力增加(P<0.05),表明miR-182可改善PCB1254对RGC-5细胞凋亡及增殖功能的影响。结论:PCB1254可能通过抑制miR-182的表达来影响RGC-5细胞的增殖和凋亡,进而导致视功能损害。
英文摘要:
      Objective: To study the mechanism of toxic effect of polychlorinated biphenyls PCB1254 on retinal ganglion cells (RGC-5). Methods: After RGC-5 cells were exposed to 0.125, 0.250, 0.500, 1.000 mg/L PCB1254, 0.01% methanol, and pure water, the level of miR-182 was detected in every group. In addition, by using the miR-182 mimics or miR-182 inhibitor to up-regulate or down-regulate the expression of miR-182 in RGC-5, apoptosis, proliferation,and cell cycle were observed. After the treatment with 0.5 mg/L and 1.0 mg/L PCB1254, miR-182 mimics were transfected into RGC-5 cells to observe the apoptosis and proliferation. Results: ① With the increasing concentration of PCB1254, the expression of miR-182 was declined. When the concentration was ≥0.5 mg/L, there were significant differences between experimental groups and the control group (P<0.05). ② MiR-182 silencing led to increased Caspase-3 activity in RGC-5 cells, which indicated that miR-182 silencing promoted apoptosis (P<0.05). CCK-8 assay showed that the cell viability was lower in miR-182 inhibitor group than that in the negative control group, which indicated that miR-182 silencing inhibited cell proliferation(P<0.05). There were no significant differences in cell cycle between the negative control group and the miR-182 inhibitor group(P>0.05). ③ When miR-182 were tranfected in RGC-5 exposed to 0.5 and 1.0 mg/L PCB1254, the caspase-3 activity decreased(P<0.05), and cell viability increased (P<0.05). It showed that miR-182 could improve the toxic effect of PCB1254 in cell apoptosis and proliferation. Conclusion: Our findings suggest that the PCB1254 may affect the proliferation and apoptosis of RGC-5 by inhibiting the expression of miR-182, which may lead to the damage of visual function.
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