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Signaling Pathways Regulating IL-1-induced COX-2 Expression

¹ Department of Oral and Maxillofacial Surgery, Graduate School of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; and
² Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science and Station for Collaborative Research, Kyushu University, Fukuoka, Japan

^* corresponding author, yasu{at}dent.kyushu-u.ac.jp

Interleukin-1(IL-1) stimulates the production of prostaglandin E₂ (PGE₂) in odontogenic keratocyst fibroblasts. However, the signaling pathways remain obscure. In this study, we investigated IL-1signaling pathways that regulate cyclooxygenase-2 (COX-2) expression in odontogenic keratocyst fibroblasts. IL-1increased the expression of COX-2 mRNA and protein, and PGE₂ secretion in the fibroblasts. IL-1increased the phosphorylation of extracellular signal-regulated protein kinase-1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK). PD-98059, SB-203580, SP-600125, and PDTC—which are inhibitors of ERK1/2, p38, JNK, and nuclear factor-B (NF-B), respectively—attenuated the IL-1-induced COX-2 mRNA expression and activated protein kinase C PGE₂ secretion. IL-1(PKC), and PKC inhibitor staurosporine inhibited IL-1-induced phosphorylation of ERK1/2, p38, and JNK, and decreased IL-1-induced COX-2 mRNA expression. Thus, in odontogenic keratocyst fibroblasts, IL-1may stimulate COX-2 expression both through the PKC-dependent activation of ERK1/2, p38, and JNK signaling pathways, and through the NF-B cascade.

KEY WORDS: cyclooxygenase-2 • prostaglandin E₂ • interleukin-1 • odontogenic keratocyst • fibroblasts

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