复发性流产肾虚证小鼠子宫蜕膜组织miRNA表达谱检测及生物信息学分析

目的 探讨微小RNA（microRNA，miRNA）在复发性流产（repeated spontaneous abortion，RSA）肾虚证小鼠子宫蜕膜组织中的表达特征。方法 运用基因芯片技术对所采集的正常对照组和RSA小鼠蜕膜组织进行miRNA检测，运用Genespring软件对miRNA进行筛选及功能分析。应用生物信息学方法分析差异表达的miRNA及其靶向基因在RSA发生、发展中的作用。结果 芯片检测结果显示正常对照组和RSA肾虚证组筛选出差异表达的miRNA共有63条（22条上调、41条下调），实时荧光定量PCR验证的miRNA的表达情况与miRNA芯片结果一致。京都基因与基因组百科全书通路富集分析及基因本体分析显示，其差异表达的miRNA涉及到PI3K-Akt信号通路、细胞吞噬通路、癌症通路、黏着斑通路、肌动蛋白细胞骨架调控通路、轴突导向信号、MAPK信号通路、PAP-1信号通路等。结论 RSA肾虚证小鼠子宫蜕膜组织中存在差异表达的micro RNA，可能涉及RSA肾虚证的发生、发展。

MicroRNA Expression Profile in Decidual Tissue of the Uterus in Mice with Recurrent Spontaneous Abortion with Kidney Deficiency Syndrome and a Bioinformatics Analysis

Objective To investigate the expression characteristics of microRNAs (miRNAs) in the decidual tissue of the uterus in mice with recurrent spontaneous abortion (RSA) with kidney deficiency syndrome. Methods The gene microarray technique was used to measure miRNAs in decidual tissue samples collected from normal mice and RSA mice, and Genespring software was used for miRNA screening and functional analysis. A bioinformatics analysis was performed to investigate the role of differentially expressed miRNAs and their targeted genes in the development and progression of RSA. Results Microarray results showed 63 differentially expressed miRNAs between normal mice and RSA mice with kidney deficiency syndrome, among which 22 were upregulated and 41 were downregulated, and the expression of miRNAs was further verified by quantitative real-time PCR. The KEGG pathway enrichment analysis and the gene ontology analysis showed that the differentially expressed miRNAs were mainly involved in the PI3K-Akt signaling pathway, cytophagy pathways, cancer pathways, focal adhesion pathways, actin cytoskeleton regulatory pathways, axon guidance signals, the MAPK signaling pathways, and the PAP1 signaling pathways. Conclusion Differentially expressed miRNAs are observed in the decidual tissue of the uterus between normal mice and RSA mice with kidney deficiency syndrome, which may be involved in the development and progression of RSA with kidney deficiency syndrome.