Amphiregulin may be a new biomarker of classically activated macrophages
Amphiregulin may be a new biomarker of classically activated macrophages
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双调蛋白可能是经典活化巨噬细胞的新生物标志物
DOI：
10.1016/j.bbrc.2015.09.037
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发表时间：
2015-10-23
影响因子：
3.1
通讯作者：
Xu, Younian
中科院分区：
文献类型：
--
作者：
Meng, Chen;Liu, Guilin;Xu, Younian
双调蛋白（Areg）参与组织修复和炎症调节。巨噬细胞作为炎症反应中重要的效应细胞，可以极化为经典的（M1）或替代的（M2）活化表型，具有多种免疫功能。然而，Areg表达和巨噬细胞活化之间的关系知之甚少。在这里，我们报告，Areg显着表达在M1，而不是在M2巨噬细胞。这通过在腹腔巨噬细胞中的RT-PCR和ELISA分析以及通过评估肺泡巨噬细胞和RAW 264.7细胞中的蛋白表达来证实。TLR4（CLI-095）和MAP激酶的选择性抑制剂Erk1/2（PD98059）、JNK（SP600125）和p38（SB203580）可显著降低M1巨噬细胞中Areg的表达，表明M1巨噬细胞主要通过TLR4-MAPK途径产生Areg，这参与了M1的活化机制。当与M1巨噬细胞的经典生物标志物的产生相比时，Areg表达在时间序列上高度一致。总之，Areg可能是M1巨噬细胞的有效新生物标志物。(C)2015 Elsevier Inc. All rights reserved.
Amphiregulin (Areg) participates in tissue repair and inflammation regulation. As important effector cells in inflammation, macrophages can be polarized to classically (M1) or alternatively (M2) activated phenotype with diverse functions in immunity. However, the relationship between Areg expression and macrophage activation is poorly understood. Here we report that Areg was significantly expressed in M1 but not in M2 macrophages. This was confirmed by analyses of RT-PCR and ELISA in peritoneal macrophages, and by evaluating protein expression in alveolar macrophages and RAW264.7 cells. Selective inhibitors of TLR4 (CLI-095) and MAP kinase, including Erk1/2 (PD98059), JNK (SP600125) and p38 (SB203580), significantly reduced Areg expression in M1 macrophages, suggesting that M1 macrophages produce Areg mainly through the TLR4-MAPK pathway, which is involved in the mechanism of M1 activation. When compared with productions of classical biomarkers of M1 macrophages, Areg expression was highly consistent in time series. Taken together, Areg may be an effective new biomarker of M1 macrophages. (C) 2015 Elsevier Inc. All rights reserved.