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Inhibition of Phosphatidylinositol 3-Kinase Amplifies TEGDMA-induced Apoptosis in Primary Human Pulp Cells

¹ Department of Oral and Maxillo-Facial Sciences and
³ Department of Cellular and Molecular Biology and Pathology, University of Naples "Federico II", via S. Pansini 5, 80131-Naples, Italy; and
² Department of Operative Dentistry and Periodontology, University of Regensburg, D-93042 Regensburg, Germany;

^* corresponding author, helmut.schweikl{at}klinik.uni-regensburg.de

Cytotoxicity of triethylene glycol dimethacrylate (TEGDMA), a co-monomer of dental resinous restorative materials, is firmly established in vitro, but the molecular mechanisms are unknown. Here we examined apoptosis and necrosis induced by TEGDMA in human primary pulp cells. The levels of apoptotic and necrotic cell populations differentially increased after exposure to increasing concentrations of TEGDMA. A two-fold increase in the percentage of apoptotic cells was induced by 1 mmol/L TEGDMA. However, a population shift among cells in apoptosis and necrosis was detected when cell cultures were exposed to 2 mmol/L TEGDMA. Inhibition of the MAP Kinase/ERK pathway had no influence on cell survival, but inhibition of phosphatidylinositol 3 kinase (PI3-Kinase; Akt/protein kinase B) by LY294002 amplified TEGDMA-induced apoptosis. Moreover, Akt phosphorylation was inhibited in the presence of TEGDMA. These results suggest that depression of PI3K signaling may be a primary target in TEGDMA-induced apoptosis.

KEY WORDS: pulp cells • apoptosis • necrosis • TEGDMA • PI3K

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