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Expression of Prostaglandin E Synthases in Periodontitis: Immunolocalization and Cellular Regulation

By Tove Båge, Anna Kats, Blanca Silva Lopez, Gareth Morgan, Gunnar Nilsson, Idil Burt, Marina Korotkova, Lisa Corbett, Alan J. Knox, Leonardo Pino, Per-Johan Jakobsson, Thomas Modéer and Tülay Yucel-Lindberg


The inflammatory mediator prostaglandin E2 (PGE2) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. The distribution of PGES in gingival tissue of patients with periodontitis and the contribution of these enzymes to inflammation-induced PGE2 synthesis in different cell types was investigated. In gingival biopsies, positive staining for PGES was observed in fibroblasts and endothelial, smooth muscle, epithelial, and immune cells. To further explore the contribution of PGES to inflammation-induced PGE2 production, in vitro cell culture experiments were performed using fibroblasts and endothelial, smooth muscle, and mast cells. All cell types expressed PGES and COX-2, resulting in basal levels of PGE2 synthesis. In response to tumor necrosis factor (TNF-α), IL-1β, and cocultured lymphocytes, however, mPGES-1 and COX-2 protein expression increased in fibroblasts and smooth muscle cells, accompanied by increased PGE2, whereas mPGES-2 and cPGES were unaffected. In endothelial cells, TNF-α increased PGE2 production only via COX-2 expression, whereas in mast cells the cytokines did not affect PGE2 enzyme expression or PGE2 production. Furthermore, PGE2 production was diminished in gingival fibroblasts derived from mPGES-1 knockout mice, compared with wild-type fibroblasts. These results suggest that fibroblasts and smooth muscle cells are important sources of mPGES-1, which may contribute to increased PGE2 production in the inflammatory condition periodontitis

Topics: Regular Article
Publisher: American Society for Investigative Pathology
OAI identifier: oai:pubmedcentral.nih.gov:3078457
Provided by: PubMed Central
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