中国组织工程研究

中国组织工程研究 ›› 2016, Vol. 20 ›› Issue (7): 925-932.doi: 10.3969/j.issn.2095-4344.2016.07.002

• 骨组织构建 bone tissue construction • 上一篇    下一篇

成骨细胞分化、骨形成与修复中转录因子Osx和Satb2的调控作用

侯秋科1，2，黄永铨3，李昀骏1，陈东风1   

  1. 1广州中医药大学，广东省广州市 510006；2广西中医药大学附属第三医院，广西壮族自治区柳州市 545001；3广东省中医院，广东省广州市 510120
  • 收稿日期:2016-01-02 出版日期:2016-02-12 发布日期:2016-02-12
  • 通讯作者: 陈东风，博士，教授，广州中医药大学，广东省广州市 510006
  • 作者简介:侯秋科，女，1983年生，广西壮族自治区柳州市人，壮族，广州中医药大学在读博士，主治医师，主要从事中医药调控干细胞防治重大疾病的研究。

Osx and Satb2 regulate osteoblast differentiation, bone formation and repair

Hou Qiu-ke1, 2, Huang Yong-quan3, Li Yun-jun1, Chen Dong-feng1   

  1. 1Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China; 2Third Affiliated Hospital of Guangxi University of Chinese Medicine, Liuzhou 545001, Guangxi Zhuang Autonomous Region, China; 3Guangdong Hospital of Traditional Chinese Medicine, Guangzhou 510120, Guangdong Province, China
  • Received:2016-01-02 Online:2016-02-12 Published:2016-02-12
  • Contact: Chen Dong-feng, M.D., Professor, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China
  • About author:Hou Qiu-ke, Studying for doctorate, Attending physician, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China; Third Affiliated Hospital of Guangxi University of Chinese Medicine, Liuzhou 545001, Guangxi Zhuang Autonomous Region, China

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812

被引次数

1

摘要：

文章快速阅读：

文题释义：

成骨细胞：在骨形成过程中要经历成骨细胞增殖、细胞外基质成熟、细胞外基质矿化和成骨细胞凋亡4个阶段，很多因素可调节这几个阶段，从而最终调控骨形成。成骨细胞增殖期成骨细胞数量增加，以形成多层细胞，并合成分泌Ⅰ型胶原以便最终可以矿化形成骨结节。对成骨细胞增殖的调控是对细胞周期的调控，包括细胞在有丝分裂原作用下复制DNA和细胞分裂的调节机制，典型的成骨细胞细胞周期时间为20-24 h。抑制与细胞周期调节相关的基因会导致增殖的停止。
骨重建：骨重建过程包括破骨细胞贴附在旧骨区域，分泌酸性物质溶解矿物质，分泌蛋白酶消化骨基质，形成骨吸收陷窝；其后成骨细胞移行至被吸收部位，分泌骨基质，骨基质矿化而形成新骨。破骨与成骨过程的平衡是维持正常骨量的关键，以至于不断地进行着骨重建。

 

背景：成骨细胞主要来自于骨髓细胞向骨基质中的间充质细胞，一些转录因子或局部因素可促进骨髓基质细胞调节分化为成骨细胞。

目的：明确C2C12细胞以及Osx与Satb2在骨质疏松修复过程中的作用。
方法：取野生型SD大鼠20只，分为正常组10只，假手术组和骨质疏松模型组(模型组)各5只，同时取Osx-KO大鼠10只。模型组和Osx-KO大鼠切除双侧卵巢构建野生型大鼠与Osx-KO大鼠进行骨质疏松模型；假手术组找出双侧卵巢但不切除。检测各组大鼠术后体质量的变化及股骨骨密度含量。体外培养C2C12细胞，并设计了siRNA-Satb2、siRNA-Osx，通过细胞实验、基因沉默、western blot法，观察成骨细胞分化的相关Osx与Satb2的表达及对骨质疏松的影响。
结果与结论：①体质量：造模12周后，模型组、Osx-KO组大鼠较正常组和假手术组大鼠显著增加(P < 0.01)。②骨密度：模型组、Osx-KO组较正常组和假手术组显著降低(P < 0.01)。③转录因子：野生型大鼠各因子均有表达，在Osx-KO大鼠中，Satb2、Osx基因的表达显著降低(P < 0.001)，而Runx2基因在两种类型的大鼠中的表达差异无显著性意义。④当对基因进行沉默后：再检测相关的成骨基因发现Satb2、Osx、Runx2、ALP基因的表达水平均有显著的抑制。⑤结果说明：在骨质疏松发病中转录因子Osx、Satb2可能是保护性分子，对成骨细胞分化、骨形成与修复有着关键的调控作用。 
ORCID: 0000-0003-3862-3791(侯秋科)

关键词: 组织构建, 成骨细胞, 骨质疏松, 转录因子, Osx, Satb2, 成骨细胞分化

Abstract:

BACKGROUND: Osteoblasts occupy an important role in osteogenesis, which mainly come from bone marrow mesenchymal cells, and some transcription factors or local factors may promote the osteogenic differentiation of bone marrow stromal cells.
OBJECTIVE: To study the role of Osx and Satb2 in C2C12 cells in the repair process of osteoporosis.
METHODS: Twenty wild-type Sprague-Dawley rats were assigned into normal control group (n=10), sham group (n=5) and osteoporosis group (model group, n=5). Another 10 Osx-KO rats were enrolled in the study. Osteoporosis models were established by removal of both ovaries in the model group and Osx-KO group. In the sham group, bilateral ovaries were exposed but not removed. Changes in body mass and femoral bone density were detected in the four groups post operation. C2C12 cells were cultured in vitro, and siRNA-Satb2 and siRNA-Osx were designed. Expressions of Osx and Satb2 and their effects on osteoporosis were observed using cell experiments, gene silencing and western blot assay.
RESULTS AND CONCLUSION: After 12 weeks, the body mass in the model and Osx-KO groups was significantly increased compared with the normal control and sham groups (P < 0.01); the bone density in the model and Osx-KO group was significantly decreased compared with the normal control and sham groups (P < 0.01). Satb2 and Osx were expressed in all the wild-type rats, but their expressions were decreased significantly in the Osx-KO rats (P < 0.001). Additionally, there was no difference in the Runx2 mRNA expression between the two kinds of rats. After silencing, the mRNA expressions of Satb2, Osx, Runx2 and ALP were all inhibited. These findings indicate that in the pathogenesis of osteoporosis, Osx and Satb2 may be protective molecules that have a regulatory role in the osteogenic differentiation, bone formation and repair.