维拉帕米
牙本质涎磷蛋白
钙通道阻滞剂
MAPK/ERK通路
牙髓干细胞
骨钙素
硅酸钙
钙
材料科学
通道阻滞剂
细胞生物学
盖髓
钙通道
蛋白激酶A
激酶
牙本质
化学
碱性磷酸酶
生物化学
成牙本质细胞
生物
间充质干细胞
复合材料
冶金
酶
作者
Buor‐Chang Wu,Chia‐Tze Kao,Tsui‐Hsien Huang,Chi-Jr Hung,Ming‐You Shie,Hsien‐Yang Chung
标识
DOI:10.1016/j.joen.2013.12.019
摘要
This study examines how calcium silicate cement extracts influence the behavior of human dental pulp cells (hDPCs) through calcium channels and active mitogen-activated protein kinase pathways, in particular extracellular signal-related kinase (ERK).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.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.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.
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