Abstract
BackgroundOsteoarthritis (OA) is a chronic joint disease and there is no a definitive cure at present. Long non-coding RNAs (lncRNAs) have been confirmed to play important roles in the development of OA. However, the underlying mechanism of lncRNA maternally expressed gene 3 (MEG3) in OA has not been well elucidated.MethodsThe rat OA model and interleukin-1β (IL-1β)-induced rat chondrocytes were constructed. The expression pattern of lncRNA MEG3 and miR-16 was detected by RT-qPCR assay in cartilage tissues of rat OA model. The effect of MEG3 and miR-16 on IL-1β-induced chondrocytes was evaluated on the basis of cell viability and apoptosis. Then, the interaction among MEG3, miR-16 SMAD7 was explored by dual-luciferase reporter assay and RIP assay.ResultsIt is found that lncRNA MEG3 was down-regulated and miR-16 was up-regulated in rat OA cartilage tissues. MEG3 knockdown promoted proliferation and inhibited apoptosis, while miR-16 knockdown suppressed proliferation and promoted apoptosis in IL-1β-induced rat chondrocytes. Moreover, MEG3 was involved in miR-16 pathway and MEG3 suppressed miR-16 expression. Additionally, SMAD7 was a target gene of miR-16 and miR-16 suppressed SMAD7 expression in IL-1β-induced chondrocytes. Moreover, the expression of SMAD7 induced by MEG3 or si-MEG3 was markedly reversed by the introduction of miR-16 or anti-miR-16. Furthermore, MEG3 exerted its anti-proliferation and pro-apoptosis by regulating miR-16 and SMAD7.ConclusionMEG3 was down-regulated and miR-16 was up-regulated in cartilage tissues of rat OA model. MEG3 knockdown might lead to the progression of OA through miR-16/SMAD7 axis.
Highlights
Osteoarthritis (OA) is a chronic joint disease and there is no a definitive cure at present
maternally expressed gene 3 (MEG3) was down-regulated and miR-16 was up-regulated in cartilage tissues of rat OA model
MEG3 knockdown might lead to the progression of OA through miR-16/SMAD7 axis
Summary
Osteoarthritis (OA) is a chronic joint disease and there is no a definitive cure at present. Long non-coding RNAs (lncRNAs) have been confirmed to play important roles in the development of OA. Osteoarthritis (OA) is a common chronic joint disease, mainly characterized by the cartilage loss, the new bone formation of joint surface as well as osteophyte formation [1]. Long non-coding RNAs (lncRNAs), a series of noncoding endogenous RNAs comprising a sequence larger than 200 nucleotides (nt), have been confirmed to play important roles in the development of inflammationrelated diseases [4]. Increasing evidences indicated that a series of lncRNAs had vital functions in the progression of OA [6], for example, HOTAIR and PCGEM1 Upregulation of HOTAIR contributes to IL-1β-induced MMP overexpression and chondrocytes apoptosis in temporomandibular joint osteoarthritis [7]. PCGEM1 stimulates proliferation of osteoarthritic synoviocytes via targeting miR-770
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