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Journal of Dental Research
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Biological

Signaling Pathways Regulating IL-1{alpha}-induced COX-2 Expression

S. Ogata1, Y. Kubota1,*, T. Yamashiro1, H. Takeuchi2, T. Ninomiya1, Y. Suyama1 and K. Shirasuna1

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

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

Interleukin-1{alpha}(IL-1{alpha}) stimulates the production of prostaglandin E2 (PGE2) in odontogenic keratocyst fibroblasts. However, the signaling pathways remain obscure. In this study, we investigated IL-1{alpha}signaling pathways that regulate cyclooxygenase-2 (COX-2) expression in odontogenic keratocyst fibroblasts. IL-1{alpha}increased the expression of COX-2 mRNA and protein, and PGE2 secretion in the fibroblasts. IL-1{alpha}increased 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-{kappa}B (NF-{kappa}B), respectively—attenuated the IL-1{alpha}-induced COX-2 mRNA expression and activated protein kinase C PGE2 secretion. IL-1{alpha}(PKC), and PKC inhibitor staurosporine inhibited IL-1{alpha}-induced phosphorylation of ERK1/2, p38, and JNK, and decreased IL-1{alpha}-induced COX-2 mRNA expression. Thus, in odontogenic keratocyst fibroblasts, IL-1{alpha}may stimulate COX-2 expression both through the PKC-dependent activation of ERK1/2, p38, and JNK signaling pathways, and through the NF-{kappa}B cascade.

Key Words: cyclooxygenase-2 • prostaglandin E2 • interleukin-1{alpha} • odontogenic keratocyst • fibroblasts

Journal of Dental Research, Vol. 86, No. 2, 186-191 (2007)
DOI: 10.1177/154405910708600215
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