Effects of Sr2+, BO33-, and SiO32- on Differentiation of Human Dental Pulp Stem Cells into Odontoblast-Like Cells

被引:4
作者
Miyano, Yuko [1 ]
Mikami, Masato [2 ]
Katsuragi, Hiroaki [2 ]
Shinkai, Koichi [3 ]
机构
[1] Nippon Dent Univ, Adv Operat Dent Endodont, Grad Sch Life Dent Niigata, Niigata, Japan
[2] Nippon Dent Univ, Dept Microbiol, Sch Life Dent Niigata, Niigata, Japan
[3] Nippon Dent Univ, Dept Operat Dent, Sch Life Dent Niigata, 1 8 Hamaura Cho, Chuo Ku, Niigata 9518580, Japan
关键词
Odontogenic differentiation; Human dental pulp stem cells; S-PRG; Borate; Strontium; Silicate; ALKALINE-PHOSPHATASE; MATRIX PROTEIN-1; OSTEOGENIC DIFFERENTIATION; IN-VITRO; TISSUE; SIALOPHOSPHOPROTEIN; DENTINOGENESIS; EXPRESSION; RESIN; MINERALIZATION;
D O I
10.1007/s12011-023-03625-z
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study aimed to clarify the effects of strontium (Sr2+), borate (BO33-), and silicate (SiO32-) on cell proliferative capacity, the induction of differentiation into odontoblast-like cells (OLCs), and substrate formation of human dental pulp stem cells (hDPSCs). Sr2+, BO33-, and SiO32- solutions were added to the hDPSC culture medium at three different concentrations, totaling nine experimental groups. The effects of these ions on hDPSC proliferation, calcification, and collagen formation after 14, 21, and 28 days of culture were evaluated using a cell proliferation assay, a quantitative alkaline phosphatase (ALP) activity assay, and Alizarin Red S and Sirius Red staining, respectively. Furthermore, the effects of these ions on hDPSC differentiation into OLCs were assessed via quantitative polymerase chain reaction and immunocytochemistry. Sr2+ and SiO32- increased the expression of odontoblast markers; i.e., nestin, dentin matrix protein-1, dentin sialophosphoprotein, and ALP genes, compared with the control group. BO33- increased the ALP gene expression and activity. The results of this study suggested that Sr2+, BO33-, and SiO32- may induce hDPSC differentiation into OLCs.
引用
收藏
页码:5585 / 5600
页数:16
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