Lin Chujiao, Zhang Qian, Yu Shuaitong, Lin Yuxiu, Li Shuchen, Liu Huan, Chen Zhi
State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory for Oral Biomedicine of Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, Wuhan, China.
State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory for Oral Biomedicine of Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Biochem Biophys Res Commun. 2018 Jan 1;495(1):493-498. doi: 10.1016/j.bbrc.2017.11.026. Epub 2017 Nov 7.
Illumination of the molecular mechanisms regulating odontoblastic differentiation of dental papilla cells is of great significance for proper dentinogenesis and dental pulp regeneration. In this study, we discovered that microRNA (miR)-3065-5p is up-regulated during odontoblastic differentiation. Overexpression of miR-3065-5p promoted odontoblastic differentiation in vitro. Dual luciferase report assay verified that miR-3065-5p could bind to the 3'UTR of bone morphogenetic protein receptor type II (BMPR2), which dramatically increased in the beginning of odontoblastic differentiation but decreased in the terminal differentiation stage. Inhibition of Bmpr2 in the early stage retarded odontoblastic differentiation while knockdown of Bmpr2 in the terminal stage enhanced odontoblastic differentiation, resembling the effect of miR-3065-5p. Taken together, our present study suggests that miR-3065-5p positively regulates odontoblastic differentiation by directly binding to Bmpr2 in the terminal differentiation stage.
阐明调节牙乳头细胞成牙本质细胞分化的分子机制,对于正常牙本质形成和牙髓再生具有重要意义。在本研究中,我们发现微小RNA(miR)-3065-5p在成牙本质细胞分化过程中上调。miR-3065-5p的过表达促进了体外成牙本质细胞的分化。双荧光素酶报告基因检测证实,miR-3065-5p可与骨形态发生蛋白受体II型(BMPR2)的3'非翻译区结合,BMPR2在成牙本质细胞分化开始时显著增加,但在终末分化阶段减少。早期抑制Bmpr2会阻碍成牙本质细胞分化,而在终末阶段敲低Bmpr2则会增强成牙本质细胞分化,类似于miR-3065-5p的作用。综上所述,我们目前的研究表明,miR-3065-5p在终末分化阶段通过直接结合Bmpr2来正向调节成牙本质细胞分化。