华西口腔医学杂志

• 专栏论著 • 上一篇    下一篇

基质细胞衍生因子-1刺激对周期性牵张力作用下ATDC5细胞的趋化因子受体4、白介素-6、胶原X表达的影响

匡斌1 王庆昱2 宋容3 孙艳燕1 柴治国4 段银钟2 戴娟2   

  1. 1.兰州市第一人民医院口腔科,兰州 730030;2.第四军医大学口腔医院正畸科,西安 710032;3.兰州大学口腔医院口腔内科,兰州 730000;4.第四军医大学口腔医院修复科,西安 710032
  • 出版日期:2014-12-01 发布日期:2014-12-01
  • 通讯作者: 段银钟,教授,博士,E-mail:duanyz@fmmu.edu.cn
  • 作者简介:匡斌,主任医师,博士,E-mail:kuangbin1223@163. com
  • 基金资助:

    国家自然科学基金资助项目(30801315)

Changes in chemokine receptor 4, interleukin-6, and collagen X expression in the ATDC5 cell line stimulated by cyclic tensile strain and stromal cell-derived factor-1

Kuang Bin1, Wang Qingyu2, Song Rong3, Sun Yanyan1, Chai Zhiguo4, Duan Yinzhong2, Dai Juan2.   

  1. 1. Dept. of Stomatology, First People’s Hospital of Lanzhou, Lanzhou 730030, China; 2. Dept. of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi’an 710032, China; 3. Dept. of Stomatology, School of Stomatology, Lanzhou University, Lanzhou 730000, China; 4. Dept. of Prosthodontics, School of Stomatology, The Fourth Military Medical University, Xi’an 710032, China
  • Online:2014-12-01 Published:2014-12-01

摘要:

目的 探讨诱导后ATDC5软骨细胞在20%形变的周期性牵张力及基质细胞衍生因子-1(SDF-1)刺激下,趋化因子受体4(CXCR4)、白介素(IL)-6及胶原X的表达变化,以期深入研究SDF-1/CXCR4信号轴在软骨细胞分化中的作用机制。方法 ATDC5细胞系经胰岛素铁硒传递蛋白(ITS)诱导3周后,分为加力和不加力两大组,每大组又分为对照组和SDF-1组。对加力组施以20%形变的拉伸力12 h。加力结束后,对各组细胞提取总蛋白,对CXCR4、IL-6及胶原X的蛋白表达进行Western blot检测。结果在不加力状态下,给予SDF-1刺激后,软骨细胞CXCR4、IL-6及胶原X的表达都出现了不同程度的增强;而在20%形变力和SDF-1的双重刺激下,此3种因子的表达出现进一步增强。结论 在异常应力作用下,SDF-1可通过上调其特异性受体CXCR4的表达进而增大与其结合的效率,最终促使SDF-1/CXCR4信号轴的激活,促进IL-6等炎症因子的表达增强,以及直接促进软骨细胞的肥大向分化,进而胶原X的表达量增高。

关键词: 颞下颌关节骨关节病, 基质细胞衍生因子-1, 趋化因子受体4, 周期性张应力

Abstract:

Objective This study further explores the stromal cell-derived factor-1 (SDF-1)/chemokine receptor 4 (CXCR4) signaling axis mechanism in temporomandibular joint osteoarthritis (OA) by detecting the changes in CXCR4, interleukin (IL)-6, and collagen X expression in the ATDC5 cell line stimulated by the cyclic tensile strain and SDF-1. Methods Insulin-transferrin-transferrin-selenium(ITS) was used to induce ATDC5 cells to differentiate into chondrocyte-like cells. After three weeks, the cells were divided into two groups: those with and without cyclic tensile strain. These groups were further divided into the negative control and SDF-1 groups. Strain force of 20% was applied. After 12 h, the total proteins were extracted from cells of the four groups, and Western blot analysis was used to detect the changes in CXCR4, IL-6, and collagen X expression. Results SDF-1 could enhance CXCR4, IL-6, and collagen X expressions in the chondrocytes, and 20% tensile strain force could further upregulate the three factors. Conclusion Under abnormal tensile force, SDF-1 can upregulate its specific receptor CXCR4, thus increasing its binding efficiency and resulting in the activation of the SDF-1/CXCR4 axis. This condition enhances the expressions of IL-6 and other inflammatory factors and directly damages to cartilage tissue. Such damage directly promotes chondrocyte hypertrophy, which enhances collagen X expression.

Key words: temporomandibular joint osteoarthritis, stromal cell-derived factor-1, chemokine receptor 4, cyclic tensile strain