MiR-146a down-regulates inflammatory response by targeting TLR3 and TRAF6 in Coxsackievirus B infection
MiR-146a down-regulates inflammatory response by targeting TLR3 and TRAF6 in Coxsackievirus B infection
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MiR-146a 通过靶向柯萨奇病毒 B 感染中的 TLR3 和 TRAF6 下调炎症反应
DOI：
10.1261/rna.071985.119
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发表时间：
2020-01-01
期刊：
影响因子：
4.5
通讯作者：
Zhong, Zhaohua
中科院分区：
文献类型：
--
作者：
Fei, Yanru;Chaulagain, Anita;Zhong, Zhaohua
柯萨奇病毒B （CVB）是人类心肌炎和扩张型心肌病的主要病因。toll样受体3 （TLR3）是一种检测病原体dsRNA的细胞内传感器。TLR3与TRAF6一起通过NF-kappa B信号通路触发炎症反应。在感染CVB3型（CVB3）的细胞中，miR-146a的丰度显著升高。miR-146a在CVB感染中的作用尚不清楚。在本研究中，TLR3和TRAF6被确定为miR-146a的靶点。升高的miR-146a抑制NF-kappa B易位，随后下调cvb3感染细胞中的促炎细胞因子表达。因此，miR-146a可以通过靶向TLR3和TRAF6双重阻断NF-kappa B通路。MiR-146a可能是炎症反应的负调节因子，是CVB感染的内在保护因子。
Coxsackievirus B (CVB) is the major cause of human myocarditis and dilated cardiomyopathy. Toll-like receptor 3 (TLR3) is an intracellular sensor to detect pathogen's dsRNA. TLR3, along with TRAF6, triggers an inflammatory response through NF-kappa B signaling pathway. In the cells infected with CVB type 3 (CVB3), the abundance of miR-146a was significantly increased. The role of miR-146a in CVB infection is unclear. In this study, TLR3 and TRAF6 were identified as the targets of miR-146a. The elevated miR-146a inhibited NF-kappa B translocation and subsequently down-regulated proinflammatory cytokine expression in the CVB3-infected cells. Therefore, the NF-kappa B pathway can be doubly blocked by miR-146a through targeting of TLR3 and TRAF6. MiR-146a may be a negative regulator on inflammatory response and an intrinsic protective factor in CVB infection.