MDPC-23 cells were incubated with ZnCl<inf>2</inf> and the levels of HO-1 protein, phosphorylated forms of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated protein kinase (ERK), c-Jun NH<inf>2</inf>-terminal kinase (JNK), and p38 were determined with western immunoblotting. The level of HO-1 mRNA was determined with RT-PCR analysis. After pretreatment with inhibitors of MAPKs, HO-1 protein level was determined in MDPC-23 cells exposed to ZnCl<inf>2</inf>. Following exposure to 500 μ M ZnCl<inf>2</inf>, the levels of both HO-1 mRNA and protein were markedly increased. The phosphorylated forms of MAPKs increased after ZnCl<inf>2</inf> exposure. Furthermore, the expression of HO-1 was markedly suppressed by treatment with the p38 inhibitor, SB203580, and mildly suppressed by the MAPK/ERK kinase inhibitor, U0126. However, treatment with the JNK inhibitor, SP600125, did not suppress ZnCl<inf>2</inf>-induced HO-1 expression. These results suggest that ZnCl<inf>2</inf> exposure induces HO-1 expression via multiple intracellular signalling pathways, including p38, ERK in this odontoblast-like cell lines.
|ジャーナル||Transactions of Japanese Society for Medical and Biological Engineering|
|出版物ステータス||Published - 2014 8 17|
ASJC Scopus subject areas
- Biomedical Engineering