LPS and TNFα induce SOCS3 mRNA and inhibit IL-6-induced activation of STAT3 in macrophages
LPS and TNFα induce SOCS3 mRNA and inhibit IL-6-induced activation of STAT3 in macrophages
复制标题
DOI：
10.1016/s0014-5793(99)01662-2
复制
发表时间：
1999-12-17
期刊：
影响因子：
3.5
通讯作者：
Graeve, L
中科院分区：
文献类型：
--
作者：
Bode, JG;Nimmesgern, A;Graeve, L
最近的研究结果表明，细胞因子信号传导可以通过同时激活的信号转导途径的其他介质来调节。在这项研究中，我们发现LPS和TNF α在人单核细胞源性巨噬细胞、大鼠肝巨噬细胞和小鼠RAW 264.7巨噬细胞中是il -6介导的STAT3激活的有效抑制剂，但在人肝癌细胞（HepG2）和大鼠肝细胞中则不是。因此，我们发现LPS和TNF α能诱导SOCS3 mRNA在两种巨噬细胞中表达，但在HepG2细胞中不表达。使用一种特定的抑制剂，有证据表明p38 MAP激酶可能参与其中，特别是对TNF α的抑制作用。(C) 1999年欧洲生化学会联合会。
Recent findings indicate that cytokine signaling can be modulated by other mediators of simultaneously activated signal transduction pathways. In this study we show that LPS and TNF alpha are potent inhibitors of IL-6-mediated STAT3 activation in human monocyte derived macrophages, rat liver macrophages and RAW 264.7 mouse macrophages but not in human hepatoma cells (HepG2) or in rat hepatocytes. Accordingly, LPS and TNF alpha were found to induce the expression of SOCS3 mRNA in each of the investigated type of macrophages but not in HepG2 cells. Using a specific inhibitor, evidence is presented that the p38 MAP kinase might be involved, especially for the inhibitory effect of TNF alpha. (C) 1999 Federation of European Biochemical Societies.