Interaction between LPS and a dental resin monomer on cell viability in mouse macrophages
| Autor: | Wolfgang Buchalla, Stephanie Krifka, Karl-Anton Hiller, Christine Petzel, Helmut Schweikl, Johannes Klement, Matthias Widbiller, Carola Bolay |
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| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Materials science Cell Survival p38 mitogen-activated protein kinases Apoptosis medicine.disease_cause Cell Line 03 medical and health sciences Mice 0302 clinical medicine medicine Animals General Materials Science Viability assay General Dentistry biology Kinase Macrophages 030206 dentistry Nitric oxide synthase Heme oxygenase Resins Synthetic 030104 developmental biology Biochemistry Mechanics of Materials biology.protein Methacrylates Reactive Oxygen Species Oxidative stress |
| Zdroj: | Dental materials : official publication of the Academy of Dental Materials. 32(12) |
| ISSN: | 1879-0097 |
| Popis: | Objective Lipopolysaccharide (LPS) from cariogenic microorganisms and resin monomers like HEMA (2-hydroxyethyl methacrylate) included in dentin adhesive are present in a clinical situation in deep dentinal cavity preparations. Here, cell survival, expression of proteins related to redox homeostasis, and viability of mouse macrophages exposed to LPS and HEMA were analyzed with respect to the influence of oxidative stress. Methods Cell survival of RAW264.7 mouse macrophages was determined using a crystal violet assay, protein expression was detected by Western blotting, and HEMA- or LPS-induced apoptosis (cell viability) was analyzed by flow cytometry. Cells were exposed to HEMA (0–8 mM), LPS (0.1 μg/ml) or combinations of both substances for 24 h. The influence of mitogen-activated protein kinases (MAPK) was analyzed using the specific inhibitors PD98059 (ERK1/2), SB203580 (p38) or SP600125 (JNK), and oxidative stress was identified by the antioxidant N -acetylcysteine (NAC). Results Cell survival was reduced by HEMA. LPS, however, increased cell survival from 29% in cultures exposed to 8 mM HEMA, to 46% in cultures co-exposed to 8 mM HEMA/LPS. Notably, LPS-induced apoptosis was neutralized by 4–6 mM HEMA but apoptosis caused by 8 mM HEMA was counteracted by LPS. Expression of NOS (nitric oxide synthase), p47 phox and p67 phox subunits of NADPH oxidase, catalase or heme oxygenase (HO-1) was associated with HEMA- or LPS-induced apoptosis. While no influence of MAPK was detected, NAC inhibited cytotoxic effects of HEMA. Significance HEMA- and LPS-triggered pathways may induce apoptosis and interfere with physiological tissue responses as a result of the differential formation of oxidative stress. |
| Databáze: | OpenAIRE |
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