表观遗传学修饰模式的改变是众多增龄性生物学行为的重要原因。随着年龄增加，牙髓细胞成牙本质细胞方向分化能力降低，与此同时，衰老牙髓细胞出现Runx2基因的表观遗传学修饰模式转变。为分析Runx2基因的表观遗传学修饰模式发生改变的机制，本项目以表观遗传修饰调控蛋白Snf5为切入点，采用RNAi和外源性表达的方法分析Snf5对衰老牙髓细胞成牙本质细胞方向分化调控的机制，重点探讨Snf5在衰老牙髓细胞Runx2基因表观遗传学修饰模式（由待调控模式转变为抑制模式）改变中的作用，通过生物芯片分析其他成牙本质细胞分化相关基因是否也被该机制调控；并进一步探讨过表达Snf5能否逆转这种抑制模式以及恢复衰老牙髓细胞的成牙本质细胞方向分化能力。本研究的结果将对衰老牙髓细胞成牙本质细胞方向分化的分子机制提供新的理论依据，并且对临床上寻找老年牙髓活髓保存方法具有重要的科学意义和潜在的应用价值。

Epigenetic mechanisms play important roles in aging-related biological processes. The odontoblastic differentiation potential decreases during cellular senescence in dental pulp cells (DPCs). Our previous study demonstrated that epigenetic modifications were involved in the transcriptional regulation of Runx2. This study is designed to identify the role of Snf5, a key epigenetic regulatory factor, in odontoblastic differentiation of senescent DPCs by RNA interference and exogenous expression, especially in the switch between the epigenetic modifications of Runx2 gene(a ‘transcription ready’ state and a ‘transcription repression’ state) by chromatin immunoprecipitation assay and bisulphate sequencing PCR. The epigenetic modifications of other odontoblastic differentiation related genes will be evaluated by the microarrays. Moreover, we will verify whether odontoblastic differentiation potential could be regained in senescent DPCs by exogenous expression of Snf5. Our research could reveal the mechanisms under odontoblastic differentiation of senescent DPCs, which is of great significance in conserving the dental pulp.