期刊
FEBS LETTERS
卷 586, 期 6, 页码 792-797出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2012.01.044
关键词
Lysophosphatidic acid; Autotaxin; LPA receptor 3; Lipopolysaccharide; THP-1 cell; CCL8
资金
- National Nature Science Foundation [31070714]
- Beijing NOVA [2005B47]
- Fundamental Research Funds for the Central Universities [105566GK]
Lysophosphatidic acid (LPA) is an important phospholipid mediator in inflammation and immunity. Previously, we showed that autotaxin (ATX), the enzyme producing LPA from lysophosphatidylcholine (LPC), is induced by LPS in THP-1 cells via the activation of PKR, JNK and p38 MAPK. In this study, we find that ATX and LPA receptor 3 (LPA(3)) are coordinately up-regulated in LPS-stimulated THP-1 cells. PKR-mediated activation of JNK1 and p38 MAPK is required for both ATX and LPA(3) up-regulation. SPK1-mediated activation of the PI3K-AKT-beta-catenin pathway is essential for ATX induction, while SPK1-mediated ERK activation is required for LPA(3) up-regulation. Either ATX or LPA(3) knock-down inhibited CCL8 induction by LPS, suggesting that ATX and LPA(3) are involved in CCL8 induction during the inflammatory process against bacterial infection. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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