Premium
Involvement of mitochondrial signalling pathway in HGFs/ S. mitis coculture response to TEGDMA treatment
Author(s) -
Gallorini Marialucia,
Sancilio Silvia,
Zara Susi,
De Colli Marianna,
Di Giulio Mara,
Cataldi Amelia,
di Giacomo Viviana
Publication year - 2014
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.35067
Subject(s) - materials science , signalling , microbiology and biotechnology , biology
Abstract Although triethylene glycol dimethacrylate (TEGDMA), a resin monomer widely used in dental practice, has been shown to have cytotoxic effects on eukaryotic cells, little is known about how the oral environment influences the cytotoxicity of this biomaterial. The aim of this study was to evaluate eukaryotic cell reaction to TEGDMA in terms of the production of reactive oxygen species (ROS), the expression of Bax, the disturbance of mitochondrial membrane potential (MMP), and the occurrence of apoptosis in an in vitro coculture model of human gingival fibroblasts (HGFs) and Streptococcus mitis strain in presence of saliva. We found that S. mitis and saliva reduced the production of ROS (from 2.2 to 1.8 fold), the occurrence of apoptosis (from 11.3 to 4.7%), and the decrease of MMP (from 0.75 to 0.9 fold) induced by TEGDMA treatment. Addition of N ‐acetylcysteine, a well known antioxidant, improved cell viability in all experimental conditions. The results obtained in this study suggest that the presence of S. mitis and saliva in the periodontal environment could protect cells against TEGDMA toxicity. These results, shedding more light on the biological and molecular events that occur in conjuction with TEGDMA treatment in vitro in a coculture model that mimics the environment of the oral cavity, confirm the key role played by oral bacteria and saliva in preventing toxic events that can occur in vivo in HGFs. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 3931–3938, 2014.