ArticlePloS one2013
Bisgma stimulates prostaglandin E2 production in macrophages via cyclooxygenase-2, cytosolic phospholipase A2, and mitogen-activated protein kinases family.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
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- Evolution of Dental Resin Adhesives-A Comprehensive Review.Journal of functional biomaterials · 2025Review
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- Assessment of Cytotoxic and Genotoxic Effect of Modern Dental MaterialsActa stomatologica Croatica · 2023Article
- In Vitro Evaluation ofMaterials (Basel, Switzerland) · 2023Article
- Meta-analytical analysis on components released from resin-based dental materials.Clinical oral investigations · 2022Review
- Biodegradation of Dental Resin-Based Composite-A Potential Factor Affecting the Bonding Effect: A Narrative Review.Biomedicines · 2022Review
- Antibacterial and Antibiofilm Properties of Three Resin-Based Dental Composites againstMaterials (Basel, Switzerland) · 2022Article
- Cytotoxic and Genotoxic Effects of Composite Resins on Cultured Human Gingival Fibroblasts.Materials (Basel, Switzerland) · 2021Article
- Evaluation of biofilm formation on novel copper-catalyzed azide-alkyne cycloaddition (CuAAC)-based resins for dental restoratives.Dental materials : official publication of the Academy of Dental Materials · 2018Article
- Simvastatin and a Plant Galactolipid Protect Animals from Septic Shock by Regulating Oxylipin Mediator Dynamics through the MAPK-cPLAMolecular medicine (Cambridge, Mass.) · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBisphenol A-glycidyl-methacrylate (BisGMA) employs as a monomer in dental resins. The leakage of BisGMA from composite resins into the peripheral environment can result in inflammation via macrophage activation. Prostaglandin E2 (PGE2) is a key regulator of immunopathology in inflammatory reactions. Little is known about the mechanisms of BisGMA-induced PGE2 expression in macrophage. The aim of this study was to evaluate the signal transduction pathways of BisGMA-induced PGE2 production in murine RAW264.7 macrophages. METHODOLOGY/PRINCIPAL
findingsHerein, we demonstrate that BisGMA can exhibit cytotoxicity to RAW264.7 macrophages in a dose- and time-dependent manner (p<0.05). In addition, PGE2 production, COX-2 expression, and cPLA2 phosphorylation were induced by BisGMA on RAW264.7 macrophages in a dose- and time-dependent manner (p<0.05). Moreover, BisGMA could induce the phosphorylation of ERK1/2 pathway (MEK1/2, ERK1/2, and Elk), p38 pathway (MEK3/6, p38, and MAPKAPK2), and JNK pathway (MEK4, JNK, and c-Jun) in a dose- and time-dependent manner (p<0.05). Pretreatment with AACOCF3, U0126, SB203580, and SP600125 significantly diminished the phosphorylation of cPLA2, ERK1/2, p38, and JNK stimulated by BisGMA, respectively (p<0.05). BisGMA-induced cytotoxicity, cPLA2 phosphorylation, PGE2 generation, and caspases activation were reduced by AACOCF3, U0126, SB203580, and SP600125, respectively (p<0.05).
conclusionsThese results suggest that BisGMA induced-PGE2 production may be via COX-2 expression, cPLA2 phosphorylation, and the phosphorylation of MAPK family. Cytotoxicity mediated by BisGMA may be due to caspases activation through the phosphorylation of cPLA2 and MAPKs family.
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