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J. Biol. Chem., Vol. 276, Issue 7, 5360-5367, February 16, 2001

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Activation of Mitogen-activated Protein Kinase p38 and Extracellular Signal-regulated Kinase Is Involved in Glass Fiber-induced Tumor Necrosis Factor- Production in Macrophages^*

Jianping Ye, Patti Zeidler, Shih-houng Young, Anthony Martinez^§, Victor A Robinson, William Jones^¶, Paul Baron^§, Xianglin Shi, and Vincent Castranova

From the National Institute for Occupational Safety and Health,  Health Effects Laboratory Division and the ^¶ Division of Respiratory Disease Studies, Morgantown, West Virginia 26505 and the ^§ Division of Applied Research and Technology, Cincinnati, Ohio 45226

In a previous study, we demonstrated that the length of glass fibers was a critical determinant of fiber potency in induction of tumor necrosis factor (TNF)- and that activation of NF-B was an important factor in this response. In the present study, we analyzed the role of mitogen-activated protein (MAP) kinases in the induction of TNF- by glass fibers. Glass fibers induced phosphorylation of MAP kinases, p38, and ERK in primary rat alveolar macrophages, and this phosphorylation was associated with TNF- gene expression. Long fibers were more potent than short fibers in activation of MAP kinases. Results from mechanistic analysis support that MAP kinases activate transcription factor c-Jun. The activated c-Jun acts on the TNF- gene promoter through two binding sites, the cyclic AMP response element and the activator protein 1-binding site. These results suggest that in addition to the NF-B pathway for TNF- production, glass fibers are able to activate c-Jun through MAP kinase pathways that lead to induction of TNF- expression.

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