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J. Biol. Chem., Vol. 282, Issue 17, 12566-12573, April 27, 2007

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JNK1 Is Required for the Induction of Mkp1 Expression in Macrophages during Proliferation and Lipopolysaccharide-dependent Activation^*

Ester Sánchez-Tilló, Mónica Comalada, Jordi Xaus, Consol Farrera, Annabel F. Valledor, Carme Caelles, Jorge Lloberas, and Antonio Celada¹

From the Macrophage Biology Group and Cell Signaling Group, Institute for Research in Biomedicine and University of Barcelona, Barcelona Science Park, Josep Samitier 1-5, E-08028 Barcelona, Spain

Macrophages proliferate in the presence of their growth factor, macrophage colony-stimulating factor (M-CSF), in a process that is dependent on early and short ERK activation. Lipopolysaccharide (LPS) induces macrophage activation, stops proliferation, and delays ERK phosphorylation, thereby triggering an inflammatory response. Proliferating or activating responses are balanced by the kinetics of ERK phosphorylation, the inactivation of which correlates with Mkp1 induction. Here we show that the transcriptional induction of this phosphatase by M-CSF or LPS depends on JNK but not on the other MAPKs, ERK and p38. The lack of Mkp1 induction caused by JNK inhibition prolonged ERK-1/2 and p38 phosphorylation. The two JNK genes, jnk1 and jnk2, are constitutively expressed in macrophages. However, only the JNK1 isoform was phosphorylated and, as determined in single knock-out mice, was necessary for Mkp1 induction by M-CSF or LPS. JNK1 was also required for pro-inflammatory cytokine biosynthesis (tumor necrosis factor-, interleukin-1, and interleukin-6) and LPS-induced NO production. This requirement is independent of Mkp1 expression, as shown in Mkp1 knock-out mice. Our results demonstrate a critical role for JNK1 in the regulation of Mkp1 induction and in LPS-dependent macrophage activation.

Received for publication, October 13, 2006 , and in revised form, February 12, 2007.

^* This work was supported by Grants BFU2004-05725/BMC (to A. C.) and BFU2004-02096 (to C. C.) from the Ministerio de Ciencia y Tecnología. 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.

¹ To whom correspondence should be addressed: Inst. for Research in Biomedicine, Barcelona Science Park, C/Josep Samitier 1-5, E-08028 Barcelona, Spain. Tel.: 34-93-403-71-65; Fax: 34-93-403-47-47; E-mail: acelada{at}ub.edu.

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