Key Laboratory for Experimental Teratology of the Ministry of Education, Department of Immunology, Shandong University Medical School, Jinan, Shandong, China.
FEBS Lett. 2012 Apr 24;586(8):1201-7. doi: 10.1016/j.febslet.2012.03.011. Epub 2012 Mar 23.
Ligation of TLR4 with LPS in macrophages leads to the production of proinflammatory cytokines, which are central to eliminate viral and bacterial infection. However, uncontrolled TLR4 activation may contribute to pathogenesis of inflammatory diseases such as septic shock. In this study, we found microRNA-210 was induced in murine macrophages by LPS. Transfection of miR-210 mimics significantly inhibited LPS-induced production of inflammatory cytokines. In contrast, transfection of anti-miR-210 inhibitors increased LPS-induced expression of proinflammatory cytokines. Furthermore, we demonstrated that miR-210 targets NF-κB1. Therefore, our data identify miR-210 as a very important feedback negative regulator for LPS-induced production of proinflammatory cytokines.
TLR4 在巨噬细胞中的 LPS 交联导致促炎细胞因子的产生，这对于消除病毒和细菌感染至关重要。然而，TLR4 的不受控制的激活可能导致炎症性疾病如败血症休克的发病机制。在这项研究中，我们发现 LPS 可诱导小鼠巨噬细胞中 microRNA-210 的产生。miR-210 模拟物的转染可显著抑制 LPS 诱导的促炎细胞因子的产生。相反，抗 miR-210 抑制剂的转染增加了 LPS 诱导的促炎细胞因子的表达。此外，我们证明 miR-210 靶向 NF-κB1。因此，我们的数据将 miR-210 鉴定为 LPS 诱导的促炎细胞因子产生的一个非常重要的负反馈调节因子。
