- 作者：Buor-Chang Wu ; DDS ; MD&lowast ; ; &dagger ; ; Chia-Tze Kao ; DDS ; MD ; PhD&lowast ; ; &dagger ; ; Tsui-Hsien Huang ; DDS ; MD ; PhD&lowast ; ; &dagger ; ; Chi-Jr Hung ; DDS ; MD&lowast ; ; &dagger ; ; Ming-You Shie ; PhD&Dagger ; ; eviltacasi@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Hsien-Yang Chung ; DDS ; MD ; PhD§ ;
- 关键词：Calcium channel blocker ; calcium silicate cement ; human dental pulp cells ; MAPK ; odontogenic differentiation ; verapamil
- 刊名：Journal of Endodontics
- 出版年：2014
- 出版时间：August 2014
- 年：2014
- 卷：40
- 期：8
- 页码：1105-1111
- 全文大小：2361 K
Methods
HDPCs are treated with various silicon concentrations both with and without verapamil, after which the cells’ viability and odontogenic differentiation markers are determined by using PrestoBlue assay and Western blot, respectively.
Results
The silicon promoted cell proliferation and inhibited calcium channel blockers. It was also found that silicon increased ERK and p38 activity in a dose-dependent manner. Furthermore, it raised the expression and secretion of alkaline phosphatase, osteocalcin, dentin sialophosphoprotein, and dentin matrix protein-1. In addition, statistically significant differences (P < .05) have been found in the secretion of osteocalcin in ERK inhibitor + verapamil between the silicon concentrations; these varations are dose-dependent and indicate that ERK signaling is involved in the silicon-induced odontogenic differentiation of hDPCs.
Conclusions
The current study shows that silicon ions released from calcium silicate substrates play a key role in odontoblastic differentiation of hDPCs through calcium channels and modulate ERK activation.