组蛋白去甲基化酶FBXL11抑制牙髓干细胞成骨和成牙本质分化  

Histone demethylase FBXL11 inhibited the osteogenic and dentinogenic differentiation potential of dental pulp stem cells

作　　者：付晓茹[1,2] 杜娟[1] 范志朋[1] 

机构地区：[1]首都医科大学口腔医学院口腔医学研究所全牙再生及口腔组织功能重建北京市重点实验室,北京100050 [2]北京市丰台区铁营医院

出　　处：《北京口腔医学》2013年第5期241-244,共4页Beijing Journal of Stomatology

基　　金：国家自然科学基金(81070798);2011年北京市"十百千"卫生人才"十"层次人选资助项目

摘　　要：目的研究组蛋白去甲基化酶FBXL11对牙髓干细胞定向分化能力的影响。方法成骨分化诱导培养基诱导牙髓干细胞体外成骨/成牙本质分化。逆转录病毒转染构建过表达FBXL11的牙髓干细胞稳定转染细胞,进行FBXL11获得性功能研究。碱性磷酸酶活性实验及碱性磷酸酶染色检测成骨/成牙本质分化早期分化指标-碱性磷酸酶活性。茜素红染色及钙离子定量分析检测牙髓干细胞体外成骨/成牙本质分化能力。实时定量RTPCR检测FBXL11及成骨/成牙本质分化相关基因-骨涎蛋白、骨桥蛋白和骨钙素的表达。结果成骨诱导牙髓干细胞抑制FBXL11的表达。过表达FBXL11明显抑制牙髓干细胞的碱性磷酸酶活性、牙髓干细胞体外矿化能力以及骨涎蛋白和骨桥蛋白的表达。结论组蛋白去甲基化酶FBXL11具有抑制牙髓干细胞成骨和成牙本质分化的潜能。Objective To investigate the role of FBXL11 （F-box and leucine-rich repeat protein 11） on the osteogenic and dentinogenic differentiation potential of dental pulp stem cells （DPSCs）.Methods Osteogenic medium was used to induce the osteogenic and dentinogenic differentiation of DPSCs.Retroviral HA-FBXL11 was used to establish the stable cells and over-expressed FBXL11 for Gain-of-function study in DPSCs.The early marker of osteogenic and dentinogenic differentiation-ALP activity was detected by alkaline phosphatase （ALP） activity assay and ALP staining.The osteogenic and dentinogenic differentiation potentials of DPSCs were investigated by alizarin-red staining and quantitative analysis of calcium in vitro.Real time RT-PCR was used to detect the osteogenesis related genes expressions,bone sialoprotein （BSP）,osteopontin （OPN） and osteocalcin （OCN）.Results The expression of FBXL11 was down-regulated after osteogenic induction.Over-expression of FBXL11 inhibited ALP activity,mineralization,the expressions of bone sialoprotein （BSP） and osteopontin （OPN） in DPSCs.Conclusion Histone demethylase FBXL11 inhibited the osteogenic and dentinogenic differentiation potential of DPSCs.

关 键 词：组蛋白去甲基化酶 牙髓干细胞 成骨 成牙本质分化 FBXL11 

分 类 号：R780.2[医药卫生—口腔医学]