Abnormal expression of miR-4784 in chondrocytes of osteoarthritis and associations with chondrocyte hyperplasia

The aim of the present study was to assess the expression of microRNA (miRNA)-4784 in the chondrocytes of early osteoarthritis (OA) and to determine the effect of double-stranded (ds)-miRNA-4784 transfection on chondrocyte function. Following the construction of an OA rabbit model, normal chondrocytes (normal control group), OA chondrocytes obtained 4 weeks after modeling (OA at week 4 group) and 8 weeks after modeling (OA at week 8 group) were used. The relative expression of miRNA-4784 in each group was detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Western blotting was performed to measure the expression of type II collagen (Col2a1) and matrix metalloproteinase (MMP)-3 in each group with or without ds-miRNA-4784 transfection. The results revealed that the levels of miR-4784 in groups OA at week 4 and 8 were significantly lower than that of normal control group (P<0.05). It was also demonstrated that Col2a1 mRNA expression levels in groups OA at week 4 and 8 were 49 and 38% of that in the normal control group, respectively. Furthermore, MMP-3 mRNA expression levels increased by 3.12- and 3.95-fold in groups OA at week 4 and 8, respectively, compared with those in the normal control group (P<0.01). Following transfection with ds-miRNA-4784, Col2a1 mRNA expression levels increased by 63 and 126% compared with the levels prior to treatment in groups OA at week 4 and 8, respectively (P<0.01). The expression levels of MMP-3 mRNA in groups OA at week 4 and 8 decreased following transfection compared with the levels prior to treatment. Col2a1 and MMP-3 protein expression exhibited similar patterns to the mRNA expression. In summary, the results of the present study suggest that miRNA-4784 expression is significantly reduced in early stage OA chondrocytes. Transfection with ds-miRNA-4784 promotes the expression of Col2a1 and inhibits the MMP-3 expression in chondrocytes.