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目的研究miR-208转染中国仓鼠肺成纤维(CHL)细胞对炎症相关靶基因程序性细胞死亡因子-4(PDCD4)的调控作用。方法运用在线数据库Targetscan.org预测前期纳米二氧化硅经气管一次性灌注大鼠实验中筛选出差异表达上调miR-208可能调控的靶基因,并进行基因本体论(GO)分析,通过文献检索选择与炎症相关的靶基因为PDCD4;分别用miR-208模拟物、模拟物阴性对照转染CHL细胞,并设空白对照组(完全培养基),测定细胞增殖率和miR-208及PDCD4的mRNA表达水平及PDCD4蛋白的表达水平。结果预测miR-208可能调控的靶基因有146个。与空白对照组相比,转染后CHL细胞的增殖率差异无统计学意义(P>0.05),miR-208 mRNA的表达增加(P<0.01),PDCD4 mRNA和蛋白的表达无统计学意义(P>0.05)。结论在CHL细胞中未见miR-208对PDCD4有间接调控作用,是否存在直接调控作用有待进一步研究。
Objective To investigate the regulatory effect of miR-208 transfected Chinese hamster lung fibroblasts (CHL) cells on programmed cell death-4 (PDCD4), an inflammation-related gene. Methods Targetscan.org was used to predict the target genes that miR-208 might upregulate by up-regulating the expression of miR-208 in the pre-traumatic rat perfused trachea with nano-silica. The gene ontology (GO) The target gene associated with inflammation was PDCD4. CHL cells were transfected with miR-208 mimics and mock negative control respectively, and blank control group (complete medium) was established. The proliferation rate of cells and the mRNA expression of miR-208 and PDCD4 Level and PDCD4 protein expression level. Results There were 146 target genes predicted to be regulated by miR-208. Compared with the blank control group, there was no significant difference in the proliferation rate of CHL cells after transfection (P> 0.05), the expression of miR-208 mRNA increased (P <0.01), and the expression of PDCD4 mRNA and protein had no statistical significance P> 0.05). Conclusion No miR-208 in CHL cells has indirect regulatory effect on PDCD4, and whether there is a direct regulatory role remains to be further studied.