牙髓干细胞（DPSCs）在牙髓损伤修复和再生过程中发挥重要作用。我们前期应用LncRNAs芯片筛选到DPSCs成牙本质向分化过程中特异表达的LncRNA CALB2，上调表达LncRNA CALB2能促进DPSCs增殖和成牙本质向分化； RNA pull-down实验筛选到LncRNA CALB2与激活Wnt通路的蛋白质GADD34相结合；生物信息学发现GADD34 3′UTR中miR-221的结合位点与LncRNA CALB2的结合序列有重叠；并且GADD34介导PP1与Axin的相互作用。因此，我们提出LncRNA CALB2能竞争miR-221结合GADD34，解除靶向抑制，上调表达的GADD34介导PP1使Axin去磷酸化，激活Wnt/β-catenin信号通路。本项目拟进一步证实这一事件并探讨其对DPSCs成牙本质向分化的重要性和意义，为临床修复牙髓损伤提供新的思路。

Dental pulp stem cells (DPSCs) play an important role in the repair and regeneration of dental pulp. In our preliminary studies, we applicated the lncRNAs microarray technology to detect and screen the specific lncRNAs in odontoblast differentiation of DPSCs. We found that lncRNA CALB2 was significantly increased in odontoblast differentiation of DPSCs. Over-expression of lncRNA CALB2 can significantly promote the proliferation and odontoblast differentiation of DPSCs. We used RNA pull-down experiments to screen and found that the lncRNA CALB2 bound with the protein GADD34 that can activate Wnt signal pathway. We applicated bioinformatics analysis and showed that miR-221 target the binding sites of lncRNA CALB2 in the 3’UTR of GADD34. And we found that the endogenous GADD34 of the cell interacted with PP1 and Axin. Therefore, we propose that lncRNA CALB2 can mediate de-repression of GADD34 by blocking miR-221, leading to GADD34 upregulation, and mediating PP1 dephosphorylation of Axin, which abnormally activating of Wnt/β-catenin signaling pathway. We intend to further confirm this event and discuss its importance and significance for proliferation and odontoblast differentiation of DPSCs, which would provide new ideas for clinical repair of pulp injury.