Department of Orthopaedics, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu Province, China.
Department of Orthopaedics, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.
J Orthop Surg Res. 2019 May 3;14(1):118. doi: 10.1186/s13018-019-1160-7.
Osteoarthritis (OA) is a prevalent degenerative disease caused by various factors. MicroRNAs are important regulators in OA. MiR-21-5p expression is decreased in OA cartilage, but the effects of modulating miR-21-5p on cartilage regeneration are unknown. Therefore, our aim was to investigate the effects of miR-21-5p on cartilage metabolism of OA chondrocytes.
We used IL-1β (10 ng/ml) to mimic OA chondrocytes. OA chondrocytes were transfected with miR-21-5p, the gene expression of COL2A1, MMP13, and ADAMTS5 was detected by qPCR. At the same time, COL2A1, MMP13, and ADAMTS5 were analyzed at the protein level by Western blot. CCK8 measured the cell's viability and SA-β-gal detected the cell's senescence.
Upregulation of miR-21-5p had increased COL2A1 expression and decreased MM P13 and ADAMTS5 expression, which were in accord with Western blot data. SA-β-gal activity significantly increased, the viability was decreased in OA chondrocytes, and upregulation of miR-21-5p can decrease the SA-β-gal activity and increase cell viability.
MiR-21-5p might be a potential disease-modifying compound in OA, as it promotes hyaline cartilage production. These results provided that novel insights into the important function in OA pathological development.
骨关节炎(OA)是一种由多种因素引起的常见退行性疾病。microRNAs 是 OA 的重要调节因子。miR-21-5p 在 OA 软骨中的表达降低,但调节 miR-21-5p 对软骨再生的影响尚不清楚。因此,我们的目的是研究 miR-21-5p 对 OA 软骨细胞软骨代谢的影响。
我们使用 IL-1β(10ng/ml)模拟 OA 软骨细胞。用 miR-21-5p 转染 OA 软骨细胞,通过 qPCR 检测 COL2A1、MMP13 和 ADAMTS5 的基因表达。同时,通过 Western blot 分析 COL2A1、MMP13 和 ADAMTS5 的蛋白水平。CCK8 测定细胞活力,SA-β-gal 检测细胞衰老。
miR-21-5p 的上调增加了 COL2A1 的表达,降低了 MMP13 和 ADAMTS5 的表达,这与 Western blot 数据一致。SA-β-gal 活性显著增加,OA 软骨细胞活力降低,上调 miR-21-5p 可降低 SA-β-gal 活性并增加细胞活力。
miR-21-5p 可能是 OA 中的一种潜在的疾病修饰化合物,因为它促进透明软骨的产生。这些结果为 OA 病理发展的重要功能提供了新的见解。