Osteoarthritis (OA) is a conversant joint disease, which seriously threatens the health of the elderly, and even leads to disability. Long non-coding RNA-activated by transforming growth factor beta (lncRNA-ATB) has been reported in diverse cancers. However, the functions of lncRNA-ATB in OA remain uninvestigated. The current study aimed to explore the impacts of lncRNA-ATB on lipopolysaccharide (LPS)-induced inflammatory injury in ATDC5 cells and to uncover the underlying mechanism. LPS-induced ATDC5 cell injury model was constructed, and the effects of lncRNA-ATB on LPS-injured cells were explored via analyzing cell viability, apoptosis, iNOS, COX-2, and inflammatory cytokines (IL-6 and TNF-alpha). Subsequently, the relationship between lncRNA-ATB and microRNA (miR)-223 was detected, and whether miR-223 was involved in modulating LPS-induced cells injury in ATDC5 cells was investigated. Finally, MyD88/NF-kappa B and p38MAPK pathways were assessed to explore the underlying mechanism. Results showed that LPS repressed cell viability, induced apoptosis, and promoted iNOS, COX-2, IL-6 and TNF-alpha expression. Additionally, we observed that lncRNA-ATB expression was down-regulated in LPS-injured cells, and lncRNA-ATB overexpression significantly alleviated LPS-induced inflammatory injury in ATDC5 cells. Interesting results revealed that miR-223 expression was down-regulated by lncRNA-ATB and miR-223 overexpression declined the protective effect of lncRNA-ATB on LPS-injured ATDC5 cells. Further, the signaling pathway experiments showed that lncRNA-ATB inhibited MyD88/NF-kappa B and p38MAPK pathways by down-regulating miR-223 in LPS-injured cells. These data demonstrated that lncRNA-ATB protected ATDC5 cells against LPS-induced inflammatory injury by repressing MyD88/NF-kappa B and p38MAPK pathways, which was mediated by down-regulation of miR-223.
[1]Jilin Univ, Dept Orthopaed, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China.
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