摘要
目的:比较炎症微环境对于牙周膜干细胞(PDLSCs)与脐带间充质干细胞(UCMSCs)再生能力的影响。方法:通过肿瘤坏死因子-α(TNF-α)刺激模拟炎症微环境,利用增殖实验和增殖标志基因细胞周期蛋白E1(CCNE1)、细胞周期蛋白D1(CCND1)检测比较PDLSCs与UCMSCs的增殖能力,AnnexinV/PI染色检测细胞凋亡,茜素红染色及成骨分化相关基因Runt相关转录因子2(RUNX2)、骨钙素(OCN)的表达水平,检测细胞成骨分化能力。结果:TNF-α处理导致PDLSCs的增殖能力和成骨分化能力显著降低(P<0.001),凋亡细胞比例有较大升高;而TNF-α处理后UCMSCs的增殖能力和成骨分化能力仅轻度降低(P<0.001),凋亡细胞比例轻度升高。结论:与PDLSCs相比,UCMSCs对炎症微环境的抵抗能力更强。
Objective:The study aims to compare effect of inflammatory microenvironment on the regenerative capacitary of periodontal ligament stem cells(PDLSCs)andumbilical cord mesenchymal stem cells(UCMSCs).Methods:TNF-αwas applied to mimic inflammatory microenvironment.Cell proliferation assay and proliferation marker genes CCNE1,CCND1 analysis were used to compare the proliferation capacity.AnnexinV/PI staining was used to detect cellular apoptosis.Alizarin red staining and osteogenesis marker genes RUNX2,OCN analysis were used to compare the capacity of osteogenic differentiation.Results:Treatment of TNF-αresulted in an obvious decrease in the proliferation and osteogenic differentiation capacity of PDLSCs(P<0.001),while an increase in apoptosis of PDLSCs.In contract,treatment of TNF-αleaded to a mild decrease in the capacity of proliferation and osteogenic differentiation in UCMSCs,and a slight increase in cellular apoptosis.Conclusions:Comparing with PDLSCs,UCMSCs are more resistant to the influence of inflammatory microenvironment.
作者
苏晓霞
雷凤珍
王芮
林亭廷
王菲
廖立
SU Xiaoxia;LEI Fengzhen;WANG Rui;LIN Tingting;Wang Fei;LIAO Li(Department of Pediatric, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China;State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, China;Department of Orthodontics, Stomatology Hospital of Xi’an Jiaotong University College of Medicine, Xi’an 710004, China)
出处
《口腔生物医学》
2020年第2期71-75,共5页
Oral Biomedicine
基金
国家自然科学基(81600912)
四川省重点研发项目(2019YFS0311)
中央高校基本科研业务费专项资金(YJ201878)。
关键词
牙周膜干细胞
脐带间充质干细胞
炎症
肿瘤坏死因子-Α
分化
增殖
periodontal ligament stem cells
umbilical cord mesenchymal stem cells
inflammation
tumor necrosis factor-α
differentiation
proliferation