三维培养成骨细胞压应力作用下的破骨诱导机制研究

被引：2

作者：

耿远明 ^{[1
]}

申晓青 ^{[1
]}

徐平平 ^{[2
]}

机构：

[1] 南方医科大学珠江医院口腔科

[2] 广东省口腔医院·南方医科大学附属口腔医院口腔颌面外科

来源：

广东牙病防治 | 2015年 / 23卷 / 10期

基金：

广东省科技计划;

关键词：

压应力; 成骨细胞; 破骨细胞;

D O I：

暂无

中图分类号：

R78 [口腔科学];

学科分类号：

100302 [口腔临床医学];

摘要：

目的观察成骨细胞在压应力下关键基因表达的变化及对前体破骨细胞的诱导作用,揭示压应力对骨吸收的调节机制。方法将小鼠成骨细胞系MC3T3-E1加入Ⅰ型胶原凝胶三维培养系统,给予2g/cm2压应力加载,以荧光共聚焦显微镜观察细胞形态,qPCR及ELISA分析压应力加载后核因子κB受体活化因子配体(receptor activator for nuclear factor-κB ligand,RANKL)及骨保护素(osteoprotegerin,OPG)表达的变化,并以压应力下MC3T3-E1培养上清液诱导培养小鼠单核巨噬细胞RAW264.7,检测诱导培养后其抗酒石酸酸性磷酸酶(tartrateresistant acid phosphatase,TRAP)活性的变化。结果 MC3T3-E1在压应力加载条件下依然保持了明显的三维生长形态,RANKL mRNA的表达显著上调(P<0.05),OPG mRNA的表达受到抑制(P<0.05);MC3T3-E1培养上清液中RANKL的浓度上升(P<0.05),OPG浓度无明显变化(P>0.05);受压应力加载的MC3T3-E1培养上清液可促进RAW264.7 TRAP酶活性的提高(P<0.05)。结论压应力可能通过诱导成骨细胞上调RANKL表达并抑制OPG表达,以促进破骨细胞的分化。

引用

页码：509 / 513

页数：5

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