LPS-induced chemokine expression in both MyD88-dependent and -independent manners is regulated by Cot/Tp12-ERK axis in macrophages

被引：78

作者：

Bandow, Kenjiro ^{[1
]}

Kusuyama, Joji ^{[1
]}

Shamoto, Mitsuo ^{[1
]}

Kakimoto, Kyoko ^{[1
]}

Ohnishi, Tomokazu ^{[1
]}

Matsuguchi, Tetsuya ^{[1
]}

机构：

[1] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Oral Biochem, Field Dev Med, Kagoshima 8908544, Japan

来源：

FEBS LETTERS | 2012年 / 586卷 / 10期

关键词：

Macrophage; Chemokine; LPS; Cot/Tp12; ERK; TOLL-LIKE RECEPTOR; NECROSIS-FACTOR-ALPHA; FACTOR-KAPPA-B; SIGNAL-TRANSDUCTION; BINDING-PROTEIN; INTERFERON-BETA; KINASE KINASE; CELL-LINES; LIPOPOLYSACCHARIDE; ACTIVATION;

D O I：

10.1016/j.febslet.2012.04.018

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

LPS signaling is mediated through MyD88-dependent and -independent pathways, activating NF-kappa B, MAP kinases and IRF3. Cot/Tp12 is an essential upstream kinase in LPS-mediated activation of ERKs. Here we explore the roles of MyD88 and Cot/Tp12 in LPS-induced chemokine expression by studying myd88 (/) and cot/tpl2 (/) macrophages. Among the nine LPS-responsive chemokines examined, mRNA induction of ccl5, cxcl10, and cxcl13 is mediated through the MyD88-independent pathway. Notably, Cot/Tpl2-ERK signaling axis exerts negative effects on the expression of these three chemokines. In contrast, LPS-induced gene expression of ccl2, ccl7, cxcl2, cxcl3, ccl8, and cxcl9 is mediated in the MyD88-dependent manner. The Cot/Tp12-ERK axis promotes the expression of the first four and inhibits the expression of the latter two. Thus, LPS induces expression of multiple chemokines through various signaling pathways in macrophages. (c) 2012 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.

引用

页码：1540 / 1546

页数：7

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