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NF-B Protection against Apoptosis Induced by HEMA

¹ Department of Oral and Maxillofacial Sciences,
² Department of Cellular and Molecular Biology and Pathology,
³ Department of Neuroscience, Unit of Physiology, and
⁴ Department of Clinical and Experimental Medicine, University of Naples "Federico II", via S. Pansini 5, 80131-Naples, Italy; and
⁵ Department of Operative Dentistry and Periodontology, University of Regensburg, 93042-Regensburg, Germany;

^* corresponding author, gspagnuo{at}unina.it

The cytotoxicity of dental monomers has been widely investigated, but the underlying mechanisms have not been elucidated. We studied the molecular mechanisms involved in cell death induced by HEMA. In human primary fibroblasts, HEMA induced a dose-dependent apoptosis that was confirmed by the activation of caspases-8, -9, and -3. We found an increase of reactive oxygen species (ROS) and NF-B activation after HEMA exposure. Blocking of ROS production by anti-oxidants had no direct influence on apoptosis caused by HEMA, but inhibition of NF-B increased the fraction of apoptotic cells. Accordingly, mouse embryonic fibroblasts (MEF) from p65–/– mice were more susceptible to HEMA-induced apoptosis than were wild-type controls. Our results indicate that exposure to HEMA triggers apoptosis and that this mechanism is not directly dependent upon redox signaling. Nevertheless, ROS induction by HEMA activates NF-B, which exerts a protective role in counteracting apoptosis.

KEY WORDS: NF-B • HEMA • apoptosis • ROS • human fibroblasts

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