Effect Of MicroRNA-25 On IL-1β-induced Cartilage Degradation And Inflammation

Objectives: to investigate miR-25 influences IL-1β-induced ECM degradation and inflammatory cytokines synthesis and OA chondrocytes apoptosis and proliferation and to provide a theoretical basis for further researching the role of miR-25 in OA development.Methods: osteoarthritis of OA model was induced by injection of Papain and isolation of primary SD rat chondrocytes of OA. OA Chondrocytes were stimulated with interleukin-1β(IL-1β) in vitro. OA chondrocytes were transfected with miR-25 mimic and inhibitor, respectively. MiR-25, ACAN, Col2a1, TNF-α, MMP-13 expression level were tested by reverse transcription and quantitative RT-PCR and/or western blotting analysis, respectively. The apoptosis and proliferation of OA chondrocytes were detected by Annexin V-FITC/PI and cell counting kit-6(CCK-8 kit) assay.Results: miR-25 expression was significantly increased in normal and OA chondrocytes treated by IL-1β(P<0.05). ACAN and Col2a1 was down-regulated by stimulation of IL-1β. TNF-αand MMP-13 was, however, up-regulated by IL-1β. Overexpression of mi R-25 counteracted IL-β-induced down-regulation of ACAN and Col2a1 expression. Conversely, low-expression of mi R-25 significantly accelerated IL-1β-induced decrease of ACAN and Col2a1; overexpression of miR-25 leaded to down-regulation of MMP-13, TNF-α in OA chondrocytes treated with IL-1β. Suppression of miR-25 induced increase of MMP-13, TNF-α; the apoptosis rates in the cells treated with miRNA-25 mimic were significantly reduced and the chondrocytes treated with miRNA-25 inhibitor were significantly induced. Prolifera-tion rates in the chondrocytes treated with miRNA-25 mimic were significantly ascended, whereas cells treated with miRNA-25 inhibitor were significantly descended.Conclusions: miR-25 mitigates the process of pathogenesis of OA, contributing to the synthesis of aggrecan and type II collagen and repressing the production of inflammatory cytokines induced OA. Further studies of mi R-25 may present new insights into disease mechanisms and provide potential therapeutic strategy in OA.