Dentin Matrix Protein 1 Compensates for Lack of Osteopontin in Regulating Odontoblastlike Cell Differentiation after Tooth Injury in Mice
Dentin Matrix Protein 1 Compensates for Lack of Osteopontin in Regulating Odontoblastlike Cell Differentiation after Tooth Injury in Mice
复制标题
牙本质基质蛋白 1 补偿骨桥蛋白的缺乏,调节小鼠牙齿损伤后成牙本质细胞样细胞的分化
DOI:
10.1016/j.joen.2019.10.002
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发表时间:
2020
影响因子:
4.2
通讯作者:
Ohshima Hayato
中科院分区:
文献类型:
--
作者:
Saito Kotaro;Nakatomi Mitsushiro;Ohshima Hayato
IntroductionAlthough dentin matrix protein 1 (DMP1) and osteopontin (OPN) act as substrates and signaling molecules for odontoblastlike cell differentiation after tooth injury, the mutual interaction between these proteins in the mechanism of odontoblastlike cell differentiation remains to be clarified. This study aimed to elucidate the role of DMP1 and OPN in regulating odontoblastlike cell differentiation after tooth injury.MethodsA groove-shaped cavity was prepared on the mesial surface of the upper first molars in wild-type andOpnknockout (KO) mice. The demineralized paraffin sections were processed for immunohistochemistry for nestin and DMP1 andin situhybridization forDmp1. For thein vitroassay, the experiments of organ culture for evaluating dentin-pulp complex regeneration using small interfering RNA treatment were performed.ResultsOnce preexisting odontoblasts died, nestin-positive newly differentiated odontoblastlike cells were arranged along the pulp-dentin border and began to express DMP1/Dmp1. InOpnKO mice, the expression of DMP1/Dmp1was up-regulated compared with that of wild-type mice. Thein vitroassay showed that the gene suppression ofDmp1by small interfering RNA showed a tendency to decrease the differentiation rate of odontoblastlike cells from 70.1% to 52.2% in wild-type teeth. In addition, the suppression ofDmp1inOpnKO teeth tended to lead to the inhibition of odontoblastlike cell differentiation.ConclusionsThese results suggest that the expression ofDmp1is up-regulated inOpnKO mice bothin vivoandin vitro, and DMP1 compensates for the lack of OPN in regulating odontoblastlike cell differentiation after tooth injury.