Detection of miR-22, miR-140 and Bone Morphogenetic Proteins (BMP)-2 Expression Levels in Synovial Fluid of Osteoarthritis Patients Before and After Arthroscopic Debridement

被引:14
|
作者
Yang, Renjun [1 ]
Zhang, Dianying [1 ]
Yu, Kai [1 ]
Sun, Luping [1 ]
Yang, Jie [1 ]
Zhao, Chunmei [1 ]
Li, Xiang [1 ]
Chen, Yuhong [1 ]
机构
[1] Tianjin Fifth Cent Hosp, Dept Osteol, Tianjin, Peoples R China
来源
MEDICAL SCIENCE MONITOR | 2018年 / 24卷
关键词
Bone Morphogenetic Proteins; MicroRNAs; Osteoarthritis; KNEE; PAIN; CHONDROCYTES; MANAGEMENT;
D O I
10.12659/MSM.908110
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Osteoarthritis (OA) is a degenerative joint disease often present on the surface and edge of the joint and beneath cartilage forming new bone. Arthroscopy had been used for the treatment of knee OA. This study aimed to measure the expression of miR-22, miR-140, and BMP-2 in patients with OA before and after arthroscopy operation. Material/Methods: The synovial fluid of 80 patients and 60 healthy volunteers were aspirated using a syringe before OA operation and again six months post-operation in patients with OA. The total RNA was extracted and analyzed by quantitative PCR. Results: The level of miR-22 was elevated in the progression of OA. The expression of miR-140 level in the synovial fluid was significantly reduced in the patients with OA and was negatively correlated with OA severity compared to controls. Expression of miR-22 and miR-120 returned to normal levels post-operatively. BMP-2 expression was reduced in patients with OA, and returned to normal levels post-operatively. Bioinformatics analysis showed that miR-22 and miR-140 closely target with 3'-UTR of BMP-2 in different positions. The correlation between BMP-2 and miR-22 was negative. The correlation between BMP-2 and miR-140 was positive. Conclusions: The present study identified a change in miR-22, miR-140, and BMP-2 expression in the synovial fluid of patients with OA before and after arthroscopic debridement. Results provide a novel characterization of the pathogenesis and therefore underlying therapeutic target for OA.
引用
收藏
页码:863 / 868
页数:6
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