早期骨关节炎软骨下骨趋化因子信号通路的表达

Expression of chemokine signaling pathway in the subchondral bone of early experimental osteoarthritis

背景:趋化因子广泛存在于炎症反应组织当中,起诱导炎症细胞趋向炎症组织参与免疫应答的作用,大量的实验研究表明,趋化因子在骨关节炎致病过程中起了重要作用。目的:分析早期骨关节炎软骨下骨的趋化因子信号通路表达改变情况,为阐述其在骨关节炎致病机制中的重要作用提供依据。方法:30只SD大鼠随机均分为实验组和对照组。实验组切除右膝内侧半月板及内侧副韧带,对照组仅切开关节囊。于造模后1,2,4周取右膝关节标本,采用全基因表达谱芯片技术研究软骨下骨全基因表达,利用差异基因分析、信号通路分析的方法分析趋化因子信号通路的表达改变情况。结果与结论:①发现一系列与趋化因子信号通路相关的差异表达基因。②实验组与对照组相比较,趋化因子信号通路在造模后1周差异有显著性意义(P<0.05),造模后2,4周差异无显著性意义(P>0.05)。说明趋化因子信号通路在极早期膝关节骨关节炎的软骨下骨改变中起重要作用。

BACKGROUND： Chemotatic factors distribute widely in the inflammatory tissues, which can induce inflammatory ceils to participate in immune response. Large experimental results have shown that chemotatic factors exert an important role in pathogenesis of osteoarthritis. OBJECTIVE： To study the expression of chemokine signaling pathway in the subchondral bone of early experimental osteoarthritis, which provides evidences that this signaling pathway plays an important role in the pathogenesis of osteoarthritis. METHODS： Thirty Sprague-Dawley rats were equally divided into two groups： experimental group and control group. The right knee joints of rats in the experimental group underwent both medial collateral ligament transection and medial meniscectomy, while a sham operation was carried out in the control group. Rats were killed at 1, 2 and 4 weeks postsurgery to obtain the right knee joints. Total RNA of the subchondral bone was extracted, and then hybridized to Agilent Whole Rat Genome Microarray. Differentially expressed genes analysis and pathway analysis were used to study the chemokine signaling pathway. RESULTS AND CONCLUSION： （1） A set of differential expression genes known involved in the chemokine signaling pathway were found. （2） Chemokine signaling pathway was found expressed significantly in 1 week post-surgery in the experimental group as compared with the control group （P 〈 0.05）, while it showed no changes at 2 and 4 weeks postsurgery （P 〉 0.05）. Chemokine signaling pathway plays an important role in pathogenesis of very early experimental osteoarthritis.