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Updated: Aug 22, 2026
Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva
Published on: April 3, 2018
Induction of microsomal prostaglandin E synthase-1 in human gingival fibroblasts
Tülay Yucel-Lindberg1, Therese Hallström, Anna Kats
1Department of Pediatric Dentistry, Institute of Odontology, Karolinska Institutet, Box 4064, S-141 04, Huddinge, Sweden. tulay.lindberg@ofa.ki.se
Abstract:
It is well established that prostaglandin E2 (PGE2) plays an important role in inflammatory diseases including periodontitis. Previously we have reported that the inflammatory mediators interleukin-1beta, (IL-1beta) and tumor necrosis factor alpha (TNFalpha) stimulate PGE2 synthesis by inducing mRNA expression of cyclooxygenase-2 (COX-2) in human gingival fibroblasts. In present study the involvement of microsomal prostaglandin E synthase-1 (mPGES-1) in relation to PGE2 production was investigated. The results showed that IL-1beta as well as TNFalpha induced mPGES-1 mRNA and protein expression accompanied by enhanced PGE2 production in gingival fibroblasts. The anti-inflammatory steroid dexamethasone (DEX) inhibited mPGES-1 mRNA and protein expression as well as PGE2 production induced by IL-1beta or TNFalpha. The COX-2 specific inhibitor, celecoxib, in contrast to the nonspecific COX inhibitor, indomethacin, markedly reduced mPGES-1 expression induced by IL-1beta. The results demonstrate that mPGES-1 regulates PGE2 production in gingival fibroblasts stimulated by inflammatory mediators IL-1beta and TNFa. This novel pathway may be a potential target for treatment strategies of periodontal disease.
Insights
Microsomal prostaglandin E synthase-1 (mPGES-1) regulates prostaglandin E2 (PGE2) production in human gingival fibroblasts stimulated by inflammatory mediators. This pathway offers a potential therapeutic target for periodontal disease treatment.
Area of Science:
- Immunology
- Biochemistry
- Periodontology
Background:
- Prostaglandin E2 (PGE2) is a key mediator in inflammatory diseases like periodontitis.
- Interleukin-1beta (IL-1beta) and Tumor Necrosis Factor alpha (TNFalpha) induce PGE2 synthesis via cyclooxygenase-2 (COX-2) in gingival fibroblasts.
Purpose of the Study:
- To investigate the role of microsomal prostaglandin E synthase-1 (mPGES-1) in PGE2 production.
- To determine if mPGES-1 is involved in inflammatory mediator-induced PGE2 synthesis in human gingival fibroblasts.
Main Methods:
- Human gingival fibroblasts were stimulated with IL-1beta and TNFalpha.
- mRNA and protein expression of mPGES-1 were analyzed.
- PGE2 production was quantified.
- Effects of dexamethasone (DEX) and celecoxib were assessed.
Main Results:
- IL-1beta and TNFalpha significantly increased mPGES-1 mRNA and protein expression, alongside enhanced PGE2 production.
- Dexamethasone inhibited IL-1beta/TNFalpha-induced mPGES-1 expression and PGE2 production.
- The COX-2 specific inhibitor, celecoxib, reduced IL-1beta-induced mPGES-1 expression.
Conclusions:
- mPGES-1 is a critical regulator of PGE2 production in gingival fibroblasts stimulated by inflammatory mediators.
- The mPGES-1 pathway represents a novel therapeutic target for managing periodontal disease.
