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
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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
Ohshima Hayato
中科院分区:
医学2区
文献类型:
--
作者:
Saito Kotaro;Nakatomi Mitsushiro;Ohshima Hayato

文献摘要

相似文献

牙本质基质蛋白1(dentin matrix protein 1,DMP 1)和骨桥蛋白(osteopontin,OPN)是牙外伤后成牙本质样细胞分化的底物和信号分子,但它们之间的相互作用在成牙本质样细胞分化机制中的作用机制尚不清楚。本研究旨在阐明DMP 1和OPN在调节牙损伤后成牙本质细胞样细胞分化中的作用。脱矿石蜡切片行nestin和DMP 1免疫组化及DMP 1原位杂交。对于thein vitroassay,器官培养实验,用于评估牙本质牙髓复合体再生使用小干扰RNA treatment were performed.ResultsOnce预先存在的成牙本质细胞死亡,nestin阳性的新分化的成牙本质细胞样细胞排列沿着牙髓牙本质边界,并开始表达DMP 1/DMP 1。在OpnKO小鼠中,DMP 1/Dmp 1的表达较野生型小鼠上调。体外实验结果表明,用小干扰RNA抑制Dmp 1基因表达,有使野生型牙中成牙本质细胞样细胞分化率从70.1%下降到52.2%的趋势。结论OpnKO小鼠牙损伤后,成牙本质细胞样细胞分化受到抑制,而成牙本质细胞样细胞样细胞分化受到抑制。
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.