15-deoxy-Δ12,14-prostaglandin J2 regulates endogenous cot MAPK kinase kinase 1 activity induced by lipopolysaccharide

被引:27
作者
Caivano, M
Rodriguez, C
Cohen, P
Alemany, S
机构
[1] Univ Autonoma Madrid, Fac Med, CSIC, Inst Invest Biomed, E-28029 Madrid, Spain
[2] Univ Dundee, Sch Life Sci, Phosphorylat Unit, Med Res Council Prot, Dundee DD1 5EH, Scotland
关键词
D O I
10.1074/jbc.M306583200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cot is a MAPK kinase kinase that has been implicated in cellular activation and proliferation. Here, we show that the addition of lipopolysaccharide (LPS) to RAW264 macrophages induces a 10-fold increase of endogenous Cot activity, measured as MAPK kinase kinase 1 activity. Taxol, but not phorbol 12-myristate 13-acetate (PMA), induces a similar activation of Cot. A tyrosine kinase activity is involved in Cot activation by LPS. 15-Deoxy-Delta(12,14)-prostaglandin J(2), but not rosiglitazone, blocks Cot activation by LPS. Furthermore, 15-deoxyDelta(12,14)- prostaglandin J(2) also inhibited the LPS-induced Cot in vitro. However, 15-deoxy-Delta(12,14-)prostaglandin J(2) does not inhibit MAPK kinase 1 or ERK1/ERK2 activation/ phosphorylation induced by PMA and mediated by c-Raf. Considering these data, we propose that the inhibition of LPS-induced Cot activation is one mechanism by which 15-deoxy-Delta(12,14)-prostaglandin J(2) acts as an anti-inflammatory.
引用
收藏
页码:52124 / 52130
页数:7
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