MafB, a target of microRNA-155, regulates dendritic cell maturation
MafB, a target of microRNA-155, regulates dendritic cell maturation
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DOI：
10.1515/biol-2016-0006
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发表时间：
2016
影响因子：
2.2
通讯作者：
Lu Yang;Rui Li;S. Xiang;Weihua Xiao
中科院分区：
文献类型：
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作者：
Lu Yang;Rui Li;S. Xiang;Weihua Xiao
MafB是bZip转录因子的一个成员，它们具有相似的基本区域/亮氨酸拉链DNA结合基序和n端激活域。众所周知，MafB在巨噬细胞中高表达，促进髓系祖细胞向巨噬细胞分化。然而，对其在树突状细胞中的功能知之甚少。在这里，我们报道了MafB作为miR-155的靶标，调控树突状细胞的成熟，而miR-155是树突状细胞成熟和功能所必需的。在LPS诱导的DC成熟过程中，MafB和miR-155呈负相关，强制表达miR-155会降低MafB的表达。荧光素酶报告基因检测显示，mir -155可直接靶向MafB 3'UTR。此外，敲低MafB可促进DC2.4细胞的表型成熟。强制表达MafB可显著减弱过表达miR-155引起的DC2.4细胞的表型成熟。总的来说，我们的数据表明，被miR-155抑制的MafB是DC成熟的负调节因子。
Abstract MafB is a member of bZip transcription factors that share similar basic region/leucine zipper DNA binding motifs and N-terminal activation domains. It is well known that MafB is highly expressed in macrophages and promotes differentiation of myeloid progenitors into macrophage. However, little is known about its function in dendritic cells. Here, we report that MafB, as a target of miR-155, which had been reported to be required for dendritic cell maturation and function, regulated dendritic cell maturation. MafB and miR-155were reversely correlated during DC maturation induced by LPS and forced expression of miR-155 reduced MafB expression. The luciferase reporter assay showed that MafB 3’UTR was directly targeted bymiR-155. In addition, knockdown of MafB promoted the phenotypic maturation of DC2.4 cells. Forced expression of MafB could significantly attenuate the phenotypic maturation of DC2.4 cells caused by overexpression of miR-155. Overall, our data demonstrates that MafB, inhibited by miR-155, was a negative regulator of DC maturation.