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。
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-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.
出处
《华西口腔医学杂志》
CAS
CSCD
北大核心
2014年第6期592-595,共4页
West China Journal of Stomatology
基金
国家自然科学基金资助项目(30801315)
