Cytosolic Peroxiredoxin Attenuates the Activation of JNK and p38 but Potentiates That of ERK in HeLa Cells Stimulated with Tumor Necrosis Factor-α

Sang Won Kang, Tong Shin Chang, Tae Hoon Lee, Eun Seon Kim, Dae Yeul Yu, Sue Goo Rhee

Research output: Contribution to journalArticlepeer-review

74 Scopus citations

Abstract

Tumor necrosis factor-α (TNF-α) induces the activation of all three types of mitogen-activated protein kinase (MAPK): c-Jun NH 2-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-α. In vitro kinase assays as well as immunoblot analysis with antibodies specific for activated MAPKs indicated that H2O2 produced in response to TNF-α 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.

Original languageEnglish
Pages (from-to)2535-2543
Number of pages9
JournalJournal of Biological Chemistry
Volume279
Issue number4
DOIs
StatePublished - 23 Jan 2004

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