Reduced MIR130A is involved in primary immune thrombocytopenia via targeting TGFB1 and IL18
Reduced MIR130A is involved in primary immune thrombocytopenia via targeting TGFB1 and IL18
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DOI：
10.1111/bjh.12934
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发表时间：
2014-09
影响因子：
6.5
通讯作者：
Haifeng Zhao;Huiyuan Li;W. Du;Donglei Zhang;Jing Ge;F. Xue;Zeping Zhou;R. Yang
中科院分区：
文献类型：
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作者：
Haifeng Zhao;Huiyuan Li;W. Du;Donglei Zhang;Jing Ge;F. Xue;Zeping Zhou;R. Yang
microRNAs（miRNAs）在调节免疫功能和预防自身免疫性疾病中起着重要作用。获得性自身免疫性疾病免疫性血小板减少症（ITP）患者中有多种miRNAs的异常表达。然而，miRNAs在ITP发病机制中的确切机制目前还不清楚。本研究通过miRNA芯片和TaqMan真实的实时聚合酶链反应检测ITP患者外周血单个核细胞（PBMC）的miRNA表达谱。与正常对照组相比，活动性慢性ITP患者PBMC中MIR130A的表达显著降低。随后，使用双荧光素酶报告基因分析来验证MIR130A靶向转化生长因子β 1（TGFB1）和白细胞介素18（IL18）基因。此外，我们还监测了ITP患者治疗前后MIR130A及其靶基因的动态表达，并确定有效治疗后MIR130A和TGFB1的表达上调，而IL18的表达下调。总之，该研究表明，减少的MIR130A通过靶向TGFB1和IL18表达参与ITP。
MicroRNAs (miRNAs) play a vital role in the regulation of immunological functions and prevention of autoimmune disease. The abnormal expressions of several miRNAs in patients with the acquired autoimmune disease, immune thrombocytopenia (ITP), have been reported. However, the exact mechanism of miRNAs in the pathogenesis of ITP is currently not well understood. This study examined the miRNA expression profile of peripheral blood mononuclear cells (PBMCs) in ITP patients by miRNA array and TaqMan real‐time polymerase chain reaction. MIR130A expression was found to be significantly decreased in PBMCs from patients with active chronic ITP compared with that of normal controls. Subsequently, dual‐luciferase reporter gene analysis was used to validate that MIR130A targeted the transforming growth factor‐beta1 (TGFB1) and interleukin 18 (IL18) genes. In addition, we also monitored the dynamic expression of MIR130A and its targeted genes pre‐ and post‐treatment of ITP patients and determined that the expression of MIR130A and TGFB1 was up‐regulated, whereas IL18 expression was down‐regulated after effective treatment. In conclusion, this study suggests that reduced MIR130A is involved in ITP via targeting of TGFB1 and IL18 expression.