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J. Biol. Chem., Vol. 278, Issue 52, 52124-52130, December 26, 2003

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15-Deoxy-^12,14-prostaglandin J₂ Regulates Endogenous Cot MAPK Kinase Kinase 1 Activity Induced by Lipopolysaccharide^*

Matilde Caivano, Cristina Rodriguez¶, Philip Cohen, and Susana Alemany, Supported by a short-term fellowship from the European Molecular Biology Organization.¶||

From the ^¶Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas, Facultad Medicina Universidad Autónoma de Madrid, Arturo Duperier 4, 28029 Madrid, Spain and the Medical Research Council Protein Phosphorylation Unit, School of Life Sciences, University of Dundee, Dundee DD15EH, United Kingdom

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-^12,14-prostaglandin J₂, but not rosiglitazone, blocks Cot activation by LPS. Furthermore, 15-deoxy-^12,14-prostaglandin J₂ also inhibited the LPS-induced Cot in vitro. However, 15-deoxy-^12,14-prostaglandin J₂ 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-^12,14-prostaglandin J₂ acts as an anti-inflammatory.

Received for publication, June 20, 2003 , and in revised form, October 2, 2003.

^* This work was supported by grants from the Association for International Cancer Research, Fundació "La Caixa," and BMC (to S. A.) and from the United Kingdom Medical Research Council and Royal Society (to P. C.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These authors contributed equally to this work.

^|| To whom correspondence should be addressed. E-mail: salemany{at}iib.uam.es.

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