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NaF Activates MAPKs and Induces Apoptosis in Odontoblast-like Cells

Department of Hygiene and Public Health I, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan

Correspondence: ^* matsuoka{at}research.twmu.ac.jp

The cytotoxic effects of fluoride on odontoblasts are not clear. In this study, we examined whether NaF induces apoptosis in MDPC-23 odontoblast-like cells and the involvement of mitogen-activated protein kinase (MAPK) signaling pathways in NaF-induced apoptosis. MDPC-23 cells incubated with 5 mM NaF for 24 hrs exhibited caspase-3 activation, cleavage of poly(ADP-ribose) polymerase, DNA fragmentation, and an increase in cytoplasmic nucleosomes. Prior to the induction of apoptosis, all MAPKs examined were phosphorylated, but in a different manner. In contrast to the sustained phosphorylation of c-Jun NH₂-terminal kinase (JNK) and p38, NaF exposure induced a biphasic phosphorylation of extracellular signal-regulated protein kinase (ERK). NaF-induced apoptosis was markedly suppressed by treatment with the JNK inhibitor, SP600125, and mildly suppressed by the MAPK/ERK kinase inhibitor, U0126. Inhibition of p38 activity did not protect cells from apoptosis. Thus, exposure to NaF induces apoptosis in odontoblast-like cells, depending on JNK and, less significantly, ERK pathways.

Key Words: sodium fluoride • odontoblasts • MDPC-23 cells • apoptosis • MAPKs

Abbreviations: Ac-DEVD-MCA, Acetyl-Asp-Glu-Val-Asp -(4-methyl-coumaryl-7-amide) • DMSO, dimethyl sulfoxide • ERK, extracellular signal-regulated protein kinase • FBS, fetal bovine serum • JNK, c-Jun NH₂-terminal kinase • MAPKs, mitogen-activated protein kinases • MEK1/2, MAPK/ERK kinase • MK-2, MAPK-activated protein kinase-2 • NaF, sodium fluoride • PARP, poly(ADP-ribose) polymerase • SD, standard deviation

Journal of Dental Research, Vol. 88, No. 5, 461-465 (2009)
DOI: 10.1177/0022034509334771


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