华西口腔医学杂志2018，Vol.36Issue(1)：39-45,7.DOI:10.7518/hxkq.2018.01.008
赖氨酸乙酰基转移酶2A通过经典Wnt通路影响牙周膜干细胞成骨分化
K (lysine) acetyltransferase 2A affects the osteogenic differentiation of periodontal ligament stem cells through the canonical Wnt pathway
摘要
Abstract
Objective This study aims to investigate the mechanism ofK (lysine) acetyltransferase 2A (KAT2A) regulation and control on the osteogenic differentiation of periodontal ligament stem cells (PDLSCs).Methods The expression levels of KAT2A in PDLSCs were compared from each generation of the normal (H-PDLSCs) and periodontitis tissues (P-PDLSCs).The influences ofKAT2A gene interference on the osteogenic differentiation of PDLSCs were also detected.In addition,the influences of the KAT2A gene interference to the canonical Wnt pathway and ligands were detected.The upstream and downstream relationships between KAT2A and canonical Wnt pathway were also determined.Results The decreased expression of KAT2A in PDLSCs from the inflammatory tissue in each generation was compared with that in PDLSCs from the healthy tissue,and the difference was statistically significant (P＜0.05).When the KAT2A gene was disrupted,the osteogenesis ability of PDLSC was declined,and the difference was statistically significant (P＜0.05).The canonical Wnt pathway was activated,and the antagonist Dickkopf-1 (DKK-1) was reduced.After the DKK-1 addition,the osteogenic differentiation of the disturbed PDLSCs was recovered,and KAT2A was unaffected.Conclusion The KAT2A expression in PDLSCs was decreased because of perio-dontitis.The classical Wnt pathway was activated to inhibit the osteogenic differentiation of the cells.关键词
牙周膜干细胞/牙周炎/乙酰基转移酶/成骨分化/经典Wnt通路Key words
periodontal ligament stem cells/periodontitis/acetyltransferase/osteogenic differentiation/classical Wnt pathway分类
医药卫生引用本文复制引用
郭武城,程洁莉,杨征毅,张忆,何恩亮,钱钧,宋晶晶,孙晋,袁林..赖氨酸乙酰基转移酶2A通过经典Wnt通路影响牙周膜干细胞成骨分化[J].华西口腔医学杂志,2018,36(1):39-45,7.基金项目
广州市科信局科技惠民专项基金(2014Y2-00058) （2014Y2-00058）
广州市属高校科研计划科技类一般项目(2012C096) （2012C096）
Science and Technology Huimin Special Fund of Guangzhou Municipal Science and Information Bureau (2014Y2-00058) （2014Y2-00058）
General Project of Scientific Research Program of University of Guangzhou (2012C096). （2012C096）
