The effect of BisGMA on cyclooxygenase-2 expression,PGE2 production and cytotoxicity via reactive oxygen species- and MEK/ERK-dependent and -independent pathways |
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| Authors: | Mei-Chi Chang Li-Deh Lin Chiu-Po Chan Hsiao-Hua Chang Lin-I. Chen Hsueh-Jen Lin Hung-Wei Yeh Wan-Yu Tseng Po-Shuen Lin Chiu-Chun Lin Jiiang-Huei Jeng |
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| Affiliation: | 1. Biomedical Science Team, Chang Gung Institute of Technology, Taoyuan, Taiwan;2. Laboratory of Dental Pharmacology, Toxicology & Material Biocompatibility, Graduate Institute of Clinical Dentistry, National Taiwan University Medical College, National Taiwan University Hospital, Taipei, Taiwan;3. Department of Dentistry, Chang Gung Memorial Hospital, Taipei, Taiwan;4. Department of Dentistry, University of Adelaide, Australia;5. Dental Department, Show Chwan Memorial Hospital, Chang-Hua, Taiwan;6. Department of Dentistry, Chang Gung Memorial Hospital, Chang Gung University, Kaohsiung, Taiwan;1. Department of Prosthodontics, School of Stomatology, Fourth Military Medical University, Xi’an, China;2. Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA;3. Center for Stem Cell Biology and Regenerative Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA;4. Department of Mechanical Engineering, University of Maryland, Baltimore County, MD 21250, USA;1. Department of Conservative Dentistry and Periodontology, University Hospital, LMU Munich, Germany;2. Walther-Straub-Institute of Pharmacology and Toxicology, Ludwig-Maximilians-University of Munich, Nußbaumstr. 26, 80336 Munich, Germany;3. Department of Orthodontics, Ludwig-Maximilians-University of Munich, Goethestr. 70, 80336 Munich, Germany;1. Department of Biomaterials and Experimental Dentistry, University of Medical Sciences, ul Bukowska 70, 60-812 Poznań, Poland;2. School of Sport, Health & Applied Science, St Mary''s University College, Twickenham, Middlesex TW1 4SX, United Kingdom;1. School of Dentistry, The University of Manchester, Manchester, UK;2. Department of Oral and Maxillofacial Rehabilitation, King Abdulaziz University, Jeddah, Saudi Arabia;3. Prosthodontic Department, University of Jordan, Amman, Jordan;4. Manchester Institute of Biotechnology, The University of Manchester, Manchester, UK;1. KU Leuven BIOMAT, Department of Oral Health Sciences, University of Leuven & Dentistry University Hospitals Leuven, Kapucijnenvoer 7, 3000 Leuven, Belgium;2. Centre for Environmental and Health, Department of Public Health and Primary Care, University of Leuven, Kapucijnenvoer 35, 3000 Leuven, Belgium;3. Idewe, External Service for Prevention and Protection at Work, Interleuvenlaan 58, B-3001 Heverlee, Belgium;4. Polymer Chemistry and Materials, Department of Chemistry, KU Leuven (University of Leuven), Celestijnenlaan 200f – Box 2404, 3000 Leuven, Belgium;1. Department of Operative Dentistry and Periodontology, University Hospital Regensburg, D-93042 Regensburg, Germany;2. Department of Oral and Maxillofacial Science, University of Naples “Federico II”, Italy |
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| Abstract: | After operative restoration, some monomers released from dentin bonding agents or composite resin may induce tissue inflammation and affect the vitality of dental pulp. Whether BisGMA, a major monomer of composite resin, may induce prostaglandin release and cytotoxicity to pulp cells and their mechanisms awaits investigation. We found that BisGMA induced cytotoxicity to human dental pulp cells at concentrations higher than 0.075 mm as analyzed by 3-(4,5-dimethyldiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. BisGMA (0.1 mm) also stimulated ERK phosphorylation, PGE2 production, COX-2 mRNA and protein expression as well as ROS production (as indicated by an increase in cellular DCF fluorescence) in dental pulp cells. Catalase (500 and 1000 U/ml) and U0126 (10 and 20 μm, a MEK inhibitor) effectively prevented the BisGMA-induced ERK activation, PGE2 production and COX-2 expression. Moreover, catalase can protect the pulp cells from BisGMA cytotoxicity, whereas aspirin and U0126 lacked of this protective activity. These results suggest that BisGMA released from composite resin may potentially affect the vitality of dental pulp and induce pulpal inflammation via stimulation of ROS production, MEK/ERK1/2 activation and subsequent COX-2 gene expression and PGE2 production. Cytotoxicity of BisGMA to dental pulp cells is related to ROS production, but not directly mediated by MEK activation and PGE2 production. |
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