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Background  The phenotypes of osteoarthritis (OA) consist of cartilage extracellular matrix (ECM) metabolism disorder and the breakdown of cartilage homeostasis, which are induced by pro-inflammatory factors and oxidative stress. Selenoproteins regulated by selenocysteine insertion sequence binding protein 2 (SBP2) are highly effective antioxidants, but their regulatory mechanisms, particularly the involvement of miRNAs, are not fully understood.    Methods  To explore whether  miR-181a-5p  and  SBP2  are involved in OA pathogenesis, we established an IL-1β model using the chondrocyte SW1353 cell line. Next, we up- or down-regulated  SBP2  and  miRNA-181a-5p  expression in the cells. Finally, we measured the expression of  miRNA-181a-5p ,  SBP2  and three selenoproteins in OA cartilage and peripheral blood.    Results  The results showed that IL-1β increased  hsa-miR-181a-5p  and decreased  SBP2  in a time- and dose-dependent manner.  GPX1  and  GPX4 , which encode crucial glutathione peroxidase antioxidant enzymes, were up-regulated along with  SBP2  and  miR-181a-5p . Furthermore,  SBP2  showed a significant negative correlation with  miR-181a-5p  during induced ATDC5 cell differentiation. There was lower  GPX1  and  GPX4  mRNA expression and SBP2 protein expression in damaged cartilage than in smooth cartilage from the same OA sample, and  hsa-miR-181a-5p  expression on the contrary. Similar results were observed in peripheral blood. In conclusion, we have reported a novel pathway in which pro-inflammatory factors, miRNA, SBP2 and selenoproteins are associated with oxidation resistance in cartilage.    Conclusion  Overall, this study provides the first comprehensive evidence that pro-inflammatory factors cause changes in the cartilage antioxidant network and describes the discovery of novel mediators of cartilage oxidative stress and OA pathophysiology. Our data suggest that  miR-181a-5p  may be used to develop novel early-stage diagnostic and therapeutic strategies for OA.    Electronic supplementary material  The online version of this article (10.1186/s12891-018-2273-6) contains supplementary material, which is available to authorized users.

The hsa-miR-181a-5p reduces oxidation resistance by controlling SECISBP2 in osteoarthritis