NaF activates MAPKs and induces apoptosis in odontoblast-like cells

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

*この研究の対応する著者

研究成果: Article査読

83 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)461-465
ページ数5
ジャーナルJournal of Dental Research
88
5
DOI
出版ステータスPublished - 2009 5月 1
外部発表はい

ASJC Scopus subject areas

  • 歯科学(全般)

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