DFO通过HIF-1α影响CXCR4阳性牙髓细胞修复能力的研究

根据前期的研究结果及文献复习，我们得出如下假设：1. CXCR4阳性牙髓细胞（CXCR4+ DPCs）可能是牙髓在形成修复性牙本质过程中起重要作用的干/前体细胞；2. 低氧诱导因子-1α（HIF-1α）可能是牙髓损伤后启动牙髓修复反应的重要启动因子；3. 去铁胺（DFO）或许能够刺激DPCs产生HIF-1α，促进下游相关靶基因的表达并通过旁分泌作用于CXCR4+ DPCs，从而提高牙髓组织的修复功能。为验证上述假设，我们拟通过DFO作用DPCs后与CXCR4+ DPC共培养，结合RNA干扰技术，从细胞增殖，迁移、黏附及成牙本质分化四个方面来考察DFO通过HIF-1α对CXCR4+ DPCs修复能力的影响。从而可以进一步完善牙髓干细胞修复理论，并为临床开发新型盖髓剂提供理论支持。

According to the preliminary findings and literature review，we draw the following hypothesis:1. The CXCR4 positive pulp cells (CXCR4+ DPCs) may be stem/precursor cells in the formation of reparative dentin; 2.Hypoxia-inducible factor-1α (HIF-1α) may be an important initiation factor for repair reaction after injury of dental pulp; 3. Deferoxamine (DFO) may be able to stimulate DPCs produce HIF-1α and it result in expression of related downstream target genes, which enhance the repair function of CXCR4+ DPCs by paracrine. In order to prove the above hypothesis, we silence DPCs HIF-1α gene by shRNA. In the meantime, we co-cultured CXCR4+ DPCs with DPCs treated by DFO in the pre/post silence of HIF-1α gene. Finally, we will observe the repair capacity of CXCR4+ DPCs including proliferation, migration, adhesion and odontoblast differentiation. Our research can further improve dental pulp stem cells repair theory and provide theoretical support for the development of a new pulp capping agent in clinic.