کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3146733 | 1197315 | 2014 | 7 صفحه PDF | دانلود رایگان |
IntroductionThis 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).MethodsHDPCs 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.ResultsThe 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.ConclusionsThe 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.
Journal: Journal of Endodontics - Volume 40, Issue 8, August 2014, Pages 1105–1111