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目的检测microRNA-200(miR-200)家族在感染狂犬病病毒鼠脑中的表达水平,预测相关靶基因,为miR-200家族靶基因的生物学验证提供数据支持,为研究miR-200家族在狂犬病病毒感染过程中的调节机制和生物学功能奠定理论基础。方法利用MicroRNA基因芯片技术检测miR-200家族在感染狂犬病病毒鼠脑组织中的表达水平,并对其进行qRT-PCR验证;利用TargetScan、MicroCosm Targets和miRarnada等3个数据库预测miR-200的靶基因,并对靶基因进行功能和信号转导通路富集分析。结果与对照组相比,miR-200在感染狂犬病病毒的小鼠脑组织中表达水平显著下降,预测的靶基因有3154个,靶基因主要参与细胞周期、细胞因子受体结合、细胞代谢、高分子代谢和生物学调节等生物学功能(P<0.01)。参与的信号通路主要有JAK-STAT信号通路、TCR信号传导通路、轴突引导、蛋白质泛素化、Wnt信号通路、TGF-β信号通路和癌症等信号通路(P<0.05)。结论 miR-200家族在感染狂犬病病毒的鼠脑组织中表达水平显著下降,预测的靶基因在相关免疫应答中起重要作用,也可能与狂犬病病毒的感染和致病性有关。
Objective To detect the expression of microRNA-200 family in the brains of rabies virus (IBD) infected rabies virus and to predict the related target genes. To provide data support for the biological verification of target genes of miR-200 family, The mechanism of infection and the biological function of virus infection laid the theoretical foundation. Methods MicroRNA microarray was used to detect the expression of miR-200 family in rabbits infected with rabies virus and validated by qRT-PCR. The target genes of miR-200 were predicted using three databases of TargetScan, MicroCosm Targets and miRarnada , And the target gene function and signal transduction pathway enrichment analysis. Results Compared with the control group, the expression level of miR-200 in brain tissue of mice infected with rabies virus was significantly decreased. There were 3154 predicted target genes. The target genes were mainly involved in cell cycle, cytokine receptor binding, cell metabolism, high Molecular metabolism and biological regulation and other biological functions (P <0.01). The involved pathways are mainly JAK-STAT signaling pathway, TCR signaling pathway, axon guidance, protein ubiquitination, Wnt signaling pathway, TGF-beta signaling pathway and cancer signaling pathway (P <0.05). Conclusions The expression of miR-200 family in the brain tissue of rabies virus infected mice is significantly decreased. The predicted target genes play an important role in the related immune response, and may also be related to the infection and pathogenicity of rabies virus.