申请人前期研究发现，MagT1与MAPK信号通路参与调控骨髓间充质干细胞（BMMSCs）成牙本质向分化，MagTl沉默后阻碍MAPK信号通路的激活，进一步高通量基因组测序发现MagT1沉默后Hspa12a基因表达升高，Pathway分析发现Hspa12a参与MAPK信号通路。本课题因此提出假设：MagT1可能通过调节Hspa12a的表达，进而激活MAPK信号通路诱导BMMSCs成牙本质向分化。本课题拟通过构建MagTl和Hspa12a基因过表达/干扰细胞模型，结合动物实验，采用qPCR、Western blot、mircoCT扫描和免疫组化等方法，研究MagT1对Hspa12a表达的影响，探讨Hspa12a调控MAPK信号通路的作用，阐明MagT1可通过下调Hspa12a的表达，进而激活MAPK信号通路诱导BMMSCs成牙本质向分化的机制，为研究牙髓再生修复机制提供理论依据及新的研究思路。

Bone marrow mesenchymal stem cells (BMMSCs) have potential of multi-differentiation, which were suitable seed cells for pulp regeneration. In our previous study, we found that MagT1 and MAPK signaling pathway regulated the odontogenic differentiation of BMMSCs, and MagT1 silencing inhibited the activation of MAPK signaling pathway. RNA sequencing of BMMSCs undergoing odontogenic differentiation found that MagT1 silencing enhanced the gene expression of Hspa12a, which was involved in the MAPK signaling pathway revealed by pathway analysis. Thus, we speculated that MagT1 controlled the expression of Hspa12a, then regulated the odontogenic differentiation of BMMSCs through Hspa12a /MAPK signaling pathway. Through silencing or enhancing the expression of MagT1 and Hspa12a, real-time PCR, western blot, mircoCT, HE staining and immunohistochemical staining, we will investigate whether MagT1 can controlled the expression of Hspa12a, and whether Hspa12a can influence the MAPK signaling pathway which involved in the odontogenic differentiation of BMMSCs. We try to conform that MagT1 controlled the expression of Hspa12a and regulated the odontogenic differentiation of BMMSCs through Hspa12a /MAPK signaling pathway.