NaF activates MAPKs and induces apoptosis in odontoblast-like cells

H. Karube, G. Nishitai, K. Inageda, H. Kurosu, M. Matsuoka*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

89 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)461-465
Number of pages5
JournalJournal of Dental Research
Issue number5
Publication statusPublished - 2009 May 1
Externally publishedYes


  • Apoptosis
  • MAPKs
  • MDPC-23 cells
  • Odontoblasts
  • Sodium fluoride

ASJC Scopus subject areas

  • Dentistry(all)


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