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J. Biol. Chem., Vol. 279, Issue 4, 2535-2543, January 23, 2004

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Cytosolic Peroxiredoxin Attenuates The Activation Of Jnk And P38 But Potentiates That Of Erk In Hela Cells Stimulated With Tumor Necrosis Factor-^*

From the ^aLaboratory of Cell Signaling, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, the ^bCenter for Cell Signaling Research, Division of Molecular Life Science, Ewha Womans University, 11-1 Daehyun-dong, Seodaemoongu, Seoul 120-750, Korea, and the ^eLaboratory of Development & Differentiation, Functional Proteomics Laboratory, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-333, Korea

Tumor necrosis factor- (TNF-) induces the activation of all three types of mitogen-activated protein kinase (MAPK): c-Jun NH₂-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK). This cytokine also induces the production of several types of reactive oxygen species, including H₂O₂. With the use both of HeLa cells expressing wild-type or dominant negative forms of the cytosolic peroxidase peroxiredoxin II and of mouse embryonic fibroblasts deficient in this protein, we evaluated the roles of H₂O₂ in the activation of MAPKs by TNF-. In vitro kinase assays as well as immunoblot analysis with antibodies specific for activated MAPKs indicated that H₂O₂ produced in response to TNF- potentiates the activation of JNK and p38 induced by this cytokine but inhibits that of ERK. Our results also suggest that cytosolic peroxiredoxins are important regulators of TNF signaling pathways.

Received for publication, July 16, 2003 , and in revised form, November 3, 2003.

^* 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.

^c Both authors contributed equally to this work.

^d Supported by an international collaboration grant from the Korean Science and Engineering Foundation.

^f Present address: Department of Oral Biochemistry, Chonnam Dental Research Institute, College of Dentistry, Chonnam National University, 300 Yongbong-dong, Puk-gu, Gwangju 500-757, Korea.

^g Present address: Department of Food and Nutrition, College of Home Economics, Chonnam National University, 300 Yongbong-dong, Puk-gu, Gwangju 500-757, Korea.

^h To whom correspondence should be addressed: Bldg. 50, Rm. 3523, South Dr., MSC 8015, Bethesda, MD 20892. Tel.: 301-496-9646; Fax: 301-480-0357; E-mail: sgrhee{at}nih.gov.

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