STL基因敲减抑制牙髓干细胞增殖  

Knockdown of STL inhibited the proliferation of dental pulp stem cells

作　　者：史瑞棠[1] 侯本祥[1] SHI Rui-tang;HOU Ben-xiang(Department of Endodontics,Capital Medical University School of Stomatology,Beijing 100050,China)

机构地区：[1]首都医科大学口腔医学院牙体牙髓科

出　　处：《北京口腔医学》2019年第4期181-185,共5页Beijing Journal of Stomatology

基　　金：国家自然科学基金(81170952);首都医科大学附属北京口腔医院学科建设基金(18-09-11)

摘　　要：目的通过研究STL基因对牙髓干细胞(DPSCs)增殖的影响,为促进DPSCs在牙组织工程中的应用提供理论依据。方法利用慢病毒敲减DPSCs的STL基因,用CCK8法和CFSE法检测其细胞增殖能力,用碘化丙啶染色检测细胞周期的分布,用实时定量RT-PCR检测细胞周期依赖素激酶抑制剂(CDKIs)相关基因的表达。结果STL的敲减效率超过70%。敲减STL能明显抑制DPSCs的增殖,DPSCs的细胞周期阻滞于G0/G1期,CDKIs相关基因(p15^INK4B、p16^INK4A、p18^INK4C、p19^INK4D、p21^Cip1、p27^Kip1)的表达显著性上调。结论敲减STL能通过上调p15^INK4B、p16^INK4A、p18^INK4C、p19^INK4D、p21^Cip1、p27^Kip1的表达使细胞周期停滞于G0/G1期,抑制DPSCs的增殖。Objective To investigate the effect of six-twelve leukemia(STL)gene on the proliferation of dental pulp stem cells(DPSCs).Methods Lentiviral STL shRNA(STLsh)was used to knock down STL in DPSCs.The cell proliferation was assessed by cell counting Kit-8(CCK8)assay and CFSE assay.The cell cycle distribution was detected by propidium iodide staining.The mRNA levels of different cyclin-dependent kinase inhibitors(CDKIs)were examined by real-time RT-PCR assays.Results More than 70%knockdown efficiency of STL was achieved in DPSCs.The depletion of STL significantly inhibited the proliferation of DPSCs,and the cell cycle was arrested in G0/G1 phase,and the mRNA levels of CDKIs(p15^INK4B,p16^INK4A,p18^INK4C,p19^INK4D,p21^Cip1,p27^Kip1)were significantly upregulated.Conclusion The depletion of STL arrested cell cycle in G0/G1 phase and inhibited the proliferation of DPSCs by upregultating p15^INK4B,p16^INK4A,p18^INK4C,p19^INK4D,p21^Cip1 and p27^Kip1.

关 键 词：牙髓干细胞 长链非编码RNA STL基因 细胞增殖 

分 类 号：R780.2[医药卫生—口腔医学]