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Prostaglandin E₂ Regulates Interleukin-1ß-induced Matrix Metalloproteinase-3 Production in Human Gingival Fibroblasts

¹ Periodontology, Department of Hard Tissue Engineering, Graduate School, and ² Centre of Excellence Program for Frontier Research on Molecular Destruction of Tooth and Bone, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8549, Japan;

^* corresponding author, pradeepruwanpura.peri{at}tmd.ac.jp

Prostaglandin E₂ (PGE₂) exerts its biological actions via EP receptors (EP₁, EP₂, EP₃, and EP₄). In the present study, we investigated whether PGE₂ regulated interleukin (IL)-1ß-induced matrix metalloproteinase (MMP)-3 production in human gingival fibroblasts (HGF) derived from periodontally healthy subjects and diseased patients. In HGF from healthy gingiva, PGE₂ down-regulated IL-1ß-induced MMP-3 production, whereas in HGF from periodontitis patients, PGE₂ enhanced it. Butaprost (an EP₂ agonist) and ONO-AE1-329 (an EP₄ agonist) suppressed IL-1ß-induced MMP-3 production, and 17-phenyl--trinor PGE₂ (an EP₁ agonist) mimicked the PGE₂ effect in HGF from healthy and periodontally diseased tissues, respectively. Analysis of these data suggests that, in HGF from healthy tissue, IL-1ß-induced MMP-3 production is down-regulated by PGE₂ via EP₂ and EP₄ receptors, whereas in cells from periodontally diseased tissue, IL-1ß-induced MMP-3 production is up-regulated via EP₁ receptors. Different regulation of IL-1ß-induced MMP-3 production by PGE₂ between healthy and periodontally diseased tissues may be involved in the pathogenesis of periodontal disease.

KEY WORDS: human gingival fibroblasts • interleukin-1ß • matrix metalloproteinase-3 • prostaglandin E₂ • EP receptors

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