中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (6): 976-979.doi: 10.3969/j.issn.1673-8225.2011.06.007

• 骨髓干细胞 bone marrow stem cells • 上一篇    下一篇

激素对兔骨髓间充质干细胞神经递质表达的影响

王义生1，张  鑫1，张  振1，赵国强2，李月白3   

  1. 1郑州大学第一附属医院骨科，河南省高等学校临床医学重点学科开放实验室，河南省郑州市 450052
    2郑州大学基础医学院生物化学教研室，河南省郑州市  450001
    3郑州大学基础医学院微生物免疫教研室，河南省郑州市  450001
  • 收稿日期:2010-11-15 修回日期:2010-12-12 出版日期:2011-02-05 发布日期:2011-02-05
  • 作者简介:王义生，男，教授，主任医师，博士生导师，主要从事骨坏死的发病机制与防治，关节脊柱外科方面的研究。 wangyisheng@zzu.edu.cn
  • 基金资助:

    2008年度河南省科技重点攻关计划项目，项目名称：RNAi阻断骨髓干细胞PPARγ基因表达预防酒精性股骨头坏死(082102310020)。郑州大学“211工程”三期建设项目，项目名称：干细胞基础与临床研究。

Steroid effects on neurotransmitter expressions in bone marrow mesenchymal stem cells of rabbits

Wang Yi-sheng1, Zhang Xin1, Zhang Zhen1, Zhao Guo-qiang2, Li Yue-bai3   

  1. 1Departmemt of Orthopaedic Surgery, First Affiliated Hospital, Zhengzhou University, Open Laboratory of Unode Science of Clinical Medicine of Henan Province, Zhengzhou  450052, Henan Province, China
    2Department of Biochemistry, Basic Medical College, Zhengzhou University, Zhengzhou  450001, Henan Province, China
    3Department of Microbiology & Immunology, Basic Medical College, Zhengzhou University, Zhengzhou  450001, Henan Province, China
  • Received:2010-11-15 Revised:2010-12-12 Online:2011-02-05 Published:2011-02-05
  • About author:Wang Yi-sheng, Professor, Chief physician, Doctoral supervisor, Departmemt of Orthopaedic Surgery, First Affiliated Hospital, Zhengzhou University, Open Laboratory of Unode Science of Clinical Medicine of Henan Province, Zhengzhou 450052, Henan Province, China wangyisheng@zzu.edu.cn
  • Supported by:

    the Key Science and Technology Project of Henan Province in 2008, No. 082102310020*; the “211 Engineering” Third-Stage Construction Program of Zhengzhou University*

PDF

534

被引次数

37

摘要：

背景：激素性股骨头坏死的确切发病机制仍未清楚，研究发现神经系统可通过多种途径调控骨髓间充质干细胞的分化，激素可能通过影响其调控机制而引起骨坏死。
目的：观察在激素作用下，骨髓间充质干细胞中神经递质或其受体mRNA表达的变化。
方法：密度梯度离心和贴壁培养获得兔骨髓间充质干细胞。将传代培养的第3代细胞随机分为两组，实验组加入浓度为10-7 mol/L的地塞米松，对照组正常培养。分别于诱导后第4，7，11，15天，测定细胞中神经生长因子、成纤维细胞生长因子、降钙素相关基因肽受体、血管活性肠肽受体、P物质受体及过氧化物酶体增殖子活化受体γ的mRNA表达。
结果与结论：实验组神经生长因子、成纤维细胞生长因子、降钙素相关基因肽受体、血管活性肠肽受体和P物质受体的mRNA表达较对照组明显降低，而过氧化物酶体增殖子活化受体γ mRNA表达较对照组明显增高，差异均具有显著性意义(P < 0.01)，实验组各因子在不同时间点间进行比较却无明显差异(P > 0.05)。结果表明大剂量激素可使骨髓间充质干细胞中具有成骨或成血管作用的神经递质或其受体表达下降，这可能与激素性股骨头坏死发生的机制有关。

关键词: 激素, 神经递质, 骨坏死, 骨髓间充质干细胞, 骨化, 血管化

Abstract:

BACKGROUND: The precise etiopathogenesis of steroid-induced necrosis of femoral head remains unclear. Studies have demonstrated that the differentiation of bone marrow mesenchymal stem cells (BMSCs) was regulated by nervous system in various ways. The regulation mechanism could be affected by steroid to induce osteonecrosis.
OBJECTIVE: To observe the changes in neurotransmitter or its receptor mRNA expression in the BMSCs under the steroid condition.
METHODS: The rabbit BMSCs were cultivated and isolated by adherence and density gradient centrifugation. The 3rd passage of BMSCs was randomly divided into two groups. In the experimental group, the cells were treated with 10-7 mol/L dexamethasone. In the control group, the cells were normally treated without dexamethasone. The mRNA expressions of nerve growth factor (NGF),  fibroblast growth factor (FGF), calcitonin gene-related peptide receptor (CGRPR), vasoactive intestinal peptide receptor (VIPR), substance P receptor (SPR) and peroxisom proliferator-activeted receptor-γ (PPARγ) of BMSCs were detected on days 4, 7, 11, 15.
RESULTS AND CONCLUSION: The expressions of NGF mRNA, FGF mRNA, CGRPR mRNA, VIPR mRNA and SPR mRNA in the experimental group were significantly lower than that in the control group, but the expression of PPARγ mRNA increased significantly (P < 0.01). There were no significantly differences compared among the experimental groups at various time points  (P > 0.05). Results suggested that high-dose steriod could depress the expressions of the neurotransmitters or their receptors which could promote the processes of ossification or vascularization in BMSCs. This might be one of the mechanisms for the development of the steroid-induced necrosis of femoral head.

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