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miR-320a 在重症肌无力患者中下调,并通过靶向丝裂原活化蛋白激酶 1 调节炎症细胞因子的产生。

MiR-320a is downregulated in patients with myasthenia gravis and modulates inflammatory cytokines production by targeting mitogen-activated protein kinase 1.

机构信息

State Key Laboratory of Bioreactor Engineering & Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, 200237, People's Republic of China.

出版信息

J Clin Immunol. 2013 Apr;33(3):567-76. doi: 10.1007/s10875-012-9834-5. Epub 2012 Nov 30.

Abstract

Myasthenia gravis (MG) are T-cell dependent antibody-mediated autoimmune disorders, microRNAs are important regulators of human autoimmune disease pathogenesis. Here, we investigated the miRNAs expression profiles in MG for the first time and found that miR-320a was significantly downregulated in MG patients compared to normal healthy people. Meanwhile, pro-inflammatory cytokins in MG patients were overexpressed. Furthermore, we identified MAPK1 as a direct target of miR-320a. Downregulation of miR-320a induced the overexpression of pro-inflammatory cytokins through promoting COX-2 expression. This process was modulated by ERK/ NF-κB pathways. Taken together, our findings suggested that miR-320a could play a role in modulation of inflammatory cytokins production.

摘要

重症肌无力(MG)是 T 细胞依赖性抗体介导的自身免疫性疾病,microRNAs 是人类自身免疫性疾病发病机制的重要调节因子。在这里,我们首次研究了 MG 中的 miRNA 表达谱,发现与正常健康人相比,MG 患者的 miR-320a 显著下调。同时,MG 患者的促炎细胞因子过度表达。此外,我们确定 MAPK1 是 miR-320a 的直接靶标。miR-320a 的下调通过促进 COX-2 的表达诱导促炎细胞因子的过表达。这一过程受 ERK/NF-κB 途径调节。总之,我们的研究结果表明,miR-320a 可能在调节炎症细胞因子的产生中发挥作用。

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