MiR-98 promotes chondrocyte apoptosis by decreasing Bcl-2 expression in a rat model of osteoarthritis

• Published in: Acta biochimica et biophysica Sinica 2016-10, Vol.48 (10), p.923-929
• Main Authors: Wang, Jing, Chen, Lingqiang, Jin, Song, Lin, Jun, Zheng, Hongmei, Zhang, Hong, Fan, Hongtao, He, Fang, Ma, Sha, Li, Qin
• Format: Article
• Language: English
• Subjects: 3' Untranslated Regions - genetics; Animals; Apoptosis - genetics; Base Sequence; Bcl-2; Blotting, Western; Cartilage, Articular - metabolism; Chondrocytes - metabolism; Disease Models, Animal; Down-Regulation; Female; Gene Expression Regulation; Gene Knockdown Techniques; HEK293 Cells; Humans; MicroRNAs - genetics; Osteoarthritis - genetics; Osteoarthritis - metabolism; Proto-Oncogene Proteins c-bcl-2 - genetics; Proto-Oncogene Proteins c-bcl-2 - metabolism; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; Sequence Homology, Nucleic Acid; 发病机制; 大鼠模型; 细胞凋亡; 荧光素酶报告基因; 蛋白水平; 软骨组织; 骨关节炎
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmw084

Altered expression of miRNA-98 （miR-98） has been reported in osteoarthritis （OA） patients, while its role and underlying mechanisms remain elusive. In the present study, a rat model of OA was established using modified Hulth method, and the expression level of miR-98 and its effect on car- tilage degradation and cell apoptosis in OA rats were examined. The results showed that up- regulated miR-98 was observed in OA rats, and knockdown of miR-98 in OA rats resulted in an inhibitory effect on cartilage degradation and chondrocyte apoptosis. Then the potential apoptosis associated genes regulated by miR-98 were screened and examined in cartilage tissues. The target gene of miR-98 was validated by luciferase reporter assay. The data showed that the increased miR-98 was accompanied with a reduced expression of Bcl-2 at both mRNA and protein levels. Furthermore, the silencing of miR-98 in OA rats prevented the down-regulation of Bcl-2 in cartilage tissues. Finally, the luciferase reporter assay validated that Bcl-2 was the target gene of miR-98. In this study, we found that miR-98 might promote chondrocyte apoptosis and cartilage degradation by down-regulating Bcl-2 expression in the pathogenesis of OA, suggesting that miR-98 can be a potential target for the treatment of OA.