Peng Hao, Liang Du, Li Baolin, Liang Chizhang, Huang Wenhua, Lin Haibin
Pharmazie. 2017 Apr 1;72(4):223-226. doi: 10.1691/ph.2017.6890.
Osteoarthritis (OA) is one of the most common chronic degenerative diseases characterized by deterioration of articular cartilage. Many studies have demonstrated the role of microRNAs (miRNAs) in OA, but the role of miR-320a in OA remains elusive. The aim of this study was to identify the protective role of miR-320a in OA cartilage degeneration by regulating the expression of BMI-1 and RUNX-2 proteins in chondrocytes. Normal and OA chondrocytes obtained from patients were cultured in vitro. The chondrocytes (both normal and OA) were transfected with miR-320a inhibitor to investigate the effects of miR-320a on chondrocyte proliferation, and to identify the miR-320a target proteins. The results indicated that miR-320a expression was significantly higher (P<0.05) in OA chondrocytes than in normal chondrocytes. Inhibition of miR-320a effectively enhanced chondrocyte cell viability in vitro in a time-dependent manner. Inhibition of miR-320a showed a significant decrease (P<0.05) in the secretion of matrix metalloproteinase-13 (MMP-13). Furthermore, miR-320a could regulate the expression levels of BMI-1 and RUNX-2 proteins in OA chondrocytes (P<0.05). The data suggested that miR-320a protected against OA cartilage degeneration and regulated the expression levels of BMI-1 and RUNX2 proteins in chondrocytes. Our study might provide a new insight in the clinical treatment of OA.
骨关节炎（OA）是最常见的慢性退行性疾病之一，其特征为关节软骨退变。许多研究已证实微小RNA（miRNA）在OA中的作用，但miR-320a在OA中的作用仍不清楚。本研究旨在通过调节软骨细胞中BMI-1和RUNX-2蛋白的表达，确定miR-320a在OA软骨退变中的保护作用。从患者获取的正常和OA软骨细胞进行体外培养。将miR-320a抑制剂转染至软骨细胞（正常和OA），以研究miR-320a对软骨细胞增殖的影响，并鉴定miR-320a的靶蛋白。结果表明，OA软骨细胞中miR-320a的表达显著高于正常软骨细胞（P<0.05）。抑制miR-320a可有效增强体外软骨细胞的活力，且呈时间依赖性。抑制miR-320a可使基质金属蛋白酶-13（MMP-13）的分泌显著减少（P<0.05）。此外，miR-320a可调节OA软骨细胞中BMI-1和RUNX-2蛋白的表达水平（P<0.05）。数据表明，miR-320a可预防OA软骨退变，并调节软骨细胞中BMI-1和RUNX2蛋白的表达水平。我们的研究可能为OA的临床治疗提供新的见解。
