人牙髓干细胞(hDPSCs形成成牙本质样细胞的能力在牙髓损伤再生机制中具有重要意义，且牙本质涎磷蛋白(DSPP)作为检测成牙本质向分化的特异性标记物之一，其调控机制备受关注。芯片结果及验证发现hDPSCs在成牙本质样分化14天时长链非编码RNA-SNHG3显著上调，数据库和基因报告分析发现SNHG3与miR-885-5p存在作用位点，并且荧光素酶报告显示下调表达的miR-885-5p对DSPP存在调控作用。据此推测SNHG3通过吸附miR-885-5p参与对DSPP的调控。本课题拟构建SNHG3和miR-885-5p过/抑制表达的稳定细胞系以分析功能；观察SNHG3的细胞内定位，明确其调控机制；进一步探索SNHG3通过吸附miR-885-5p调控DSPP参与的调控机制。研究旨在阐明SNHG3调控hDPSCs成牙本质样分化的功能及机制，为牙髓再生提供新思路。

Attributed to the capacity of differentiation into odontoblast-like cells, human dental pulp stem cells (hDPSCs) function as crucial roles in repairment mechanism in dental pulp impairment. As a specific gene of odontoblast differentiation, dentin sialophosphoprotein (DSPP) has been a research hot spot. Microarray analysis and validation results have revealed significant up-regulation of long non-coding RNA-SNHG3 (lncRNA-SNHG3) in hDPSCs when induced into odontoblast at day 14. Based on the binding site prediction of lncRNA-SNHG3 and miR-885-5p and demonstration of negative regulatory effect of miR-885-5p on DSPP by dual-luciferase reporter assay, we propose that lncRNA-SNHG3 may regulate expression of DSPP by sponging miR-885-5p. In this study, we constructed hDPSC cell lines persistently over-/under-expressing lncRNA-SNHG3 or miR-885-5p for analysis of their functions in odontoblast differentiation of hDPSCs. Further, through detection of localization of lncRNA-SNHG3 in hDPSC, we investigate the mechanism of lncRNA-SNHG3 in regulating DSPP via miR-885-5p. This study aims to illuminate the function of lncRNA-SNHG3 in regulating odontoblast differentiation of hDPSCs to provide novel ideas for dental pulp regeneration.