NADPH oxidase 4 is involved in the triethylene glycol dimethacrylate-induced reactive oxygen species and apoptosis in human embryonic palatal mesenchymal and dental pulp cells

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• 作者：Cheng-Chang Yeh ; Jenny Zwei-Chieng Chang ; Wan-Hsien Yang…
• 关键词：TEGDMA ; Apoptosis ; NADPH oxidase 4 ; NOX4 ; Cytochrome c ; Caspase
• 刊名：Clinical Oral Investigations
• 出版年：2015
• 出版时间：July 2015
• 年：2015
• 卷：19
• 期：6
• 页码：1463-1471
• 全文大小：1,134 KB
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• 作者单位：Cheng-Chang Yeh (1)
  Jenny Zwei-Chieng Chang (1)
  Wan-Hsien Yang (1)
  Hao-Hueng Chang (1)
  Eddie Hsiang-Hua Lai (1)
  Mark Yen-Ping Kuo (1)
  
  1. School of Dentistry, College of Medicine and Department of Dentistry, National Taiwan University Hospital, National Taiwan University Medical Center, 1 Chang-Te Street, Taipei, 10048, Taiwan
  
• 刊物类别：Medicine
• 刊物主题：Dentistry
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1436-3771

文摘

Objectives Triethylene glycol dimethacrylate (TEGDMA) is a common component of resin-based dental composites and endodontic sealers. TEGDMA induces apoptosis in several types of cells. However, the mechanisms are not completely understood. The aim of this study was to investigate the mechanisms underlying TEGDMA-induced apoptosis in human embryonic palatal mesenchymal (HEPM) pre-osteoblasts and primary human dental pulp (HDP) cells. Material and methods Cell viability was examined after TEGDMA treatment. Cell cycle progression was checked by flow cytometry. Apoptotic cells were evaluated using terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling assay and visualized by fluorescence microscopy. Western blot analyses were performed to determine expressions of apoptosis-related proteins. The production of reactive oxygen species (ROS) was detected using flow cytometry. NADPH oxidase 4 (NOX4) expression levels were investigated using real-time quantitative polymerase chain reaction and Western blot analyses. Results TEGDMA increased cytosol cytochrome c levels and activated caspase-9 in HEPM and HDP cells. TEGDMA decreased the expression of anti-apoptotic protein Bcl-XL. TEGDMA-induced apoptosis was inhibited by caspase-9-specific inhibitor, anti-oxidants, NOX inhibitor, NOX4 inhibitor, and NOX4 small interfering RNA (siRNA). TEGDMA increased ROS production and upregulated NOX4 mRNA and protein expression. TEGDMA-induced intracellular ROS production was inhibited by NOX inhibitor and NOX4 inhibitor. Conclusions We demonstrate significant involvement of NOX4 in the TEGDMA-induced ROS. NOX4-derived ROS subsequently induces mitochondrial cytochrome c release leading to apoptosis through activation of the intrinsic apoptotic pathway. Clinical relevance NOX4 may be a potential target for strategies to prevent or ameliorate the TEGDMA-induced toxicity in HEPM and HDP cells.