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论文摘要

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

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

作者:匡斌 王庆昱 宋容 孙艳燕 柴治国 段银钟 戴娟

Author:Kuang Bin, Wang Qingyu, Song Rong, Sun Yanyan, Chai Zhiguo, Duan Yinzhong, Dai Juan.

收稿日期:          年卷(期)页码:2014,32(6):592-592-595

期刊名称:华西口腔医学杂志

Journal Name:West China Journal of Stomatology

关键字: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,

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

基金项目:

国家自然科学基金资助项目(30801315)

中文摘要

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。

英文摘要

ObjectiveThis 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.MethodsInsulin-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.ResultsSDF-1 could enhance CXCR4, IL-6, and collagen X expressions in the chondrocytes, and 20% tensile strain force could further upregulate the three factors.ConclusionUnder 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.

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