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目的:探讨系统性红斑狼疮(SLE)患者CD4+T细胞miR-126宿主基因EGFL7的甲基化水平对miR-126表达的调控。方法:采用实时qPCR检测SLE患者CD4+T细胞miR-126及EGFL7 mRNA表达水平;亚硫酸氢钠基因组测序法检测EGFL7基因启动子区甲基化状态。结果:miR-126及其宿主基因EGFL7在SLE患者CD4+T细胞表达上调(P<0.01),EGFL7 mRNA表达水平与miR-126的表达呈正相关(r=0.538,P=0.015)。miR-126是一个内含子miRNA,位于宿主基因EGFL7基因座第7个内含子中,其自身的基因序列中包含29个CpG位点。但该区域甲基化水平在SLE患者CD4+T细胞和正常对照组间差异无统计学意义(P=0.907)。而SLE患者CD4+T细胞中EGFL7基因启动子区甲基化水平显著降低(P<0.05)。结论:SLE患者CD4+T细胞miR-126宿主基因EGFL7启动子区甲基化状态调控宿主基因本身及其miR-126的表达。
AIM: To investigate the regulation of miR-126 expression by methylation level of miR-126 host gene EGFL7 in CD4 + T cells in patients with systemic lupus erythematosus (SLE). Methods: The real-time qPCR was used to detect the mRNA expression of miR-126 and EGFL7 in CD4 + T cells. The methylation status of EGFL7 promoter was detected by sodium bisulfite sequencing. Results: miR-126 and its host gene EGFL7 were upregulated in CD4 + T cells of SLE patients (P <0.01). The expression of EGFL7 mRNA was positively correlated with the expression of miR-126 (r = 0.538, P = 0.015). miR-126 is an intron miRNA that is located in the 7th intron of the EGFL7 locus of the host gene and contains 29 CpG sites in its own gene sequence. However, there was no significant difference in methylation level between CD4 + T cells and normal controls in SLE patients (P = 0.907). The methylation level of EGFL7 promoter in CD4 + T cells was significantly decreased in SLE patients (P <0.05). Conclusion: The methylation status of EGFL7 promoter in CD4 + T cells of SLE patients regulated the expression of host gene itself and its miR-126.