Abstract  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 cartilage 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.

Keywords   microRNA-98; osteoarthritis; Bcl-2; apoptosis

Received   2016-3-11����
Accepted  2016-7-26

Funding  This work was supported by the grant from the National Natural Science Foundation of China (No. 81260286).

* Correspondence address  Tel/Fax: +86-871-63638784; E-mail: [email protected]

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