LINC01534 promotes the aberrant metabolic dysfunction and inflammation in IL-1β-simulated osteoarthritic chondrocytes by targeting miR-140-5p

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Abstract Backgrounds: Long non-coding RNA 01534 (LINC01534) is highly expressed in the tissues of patients with osteoarthritis (OA). This study investigated the mechanism of LINC01534 on abnormal metabolic dysfunction and inflammation in OA chondro-cytes induced by IL-1β. Methods: The quantitative Real-Time PCR (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β. The ex-pressions of aggrecan and collagen II in the chondrocyte were detected by Western Blot. The levels of TNF-α, IL-8, IL-6, MMP-13, MMP-9, MMP-3 and prostaglandin E2 (PGE2) in chondrocyte were determined by ELISA. Bioinformatics, dual luciferin gene reporting, RNA pulldown and Northern Blot were used to determine the interac-tion between LINC01534 and miR-140-5p. Results: The results showed that LINC01534 was up-regulated in both OA cartilage tissue and OA chondrocyte model. In addition, silencing LINC01534 significantly alleviated the inhibitory effect of IL-1β on expressions of aggrecan and collagen II in chondrocytes, and significantly down-regulated the expression of matrix metallopro-teinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also sig-nificantly inhibited the productions of pro-inflammatory factors NO, PGE2, TNF-α, IL-6 and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was con-firmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on inflammation and abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion: Therefor, LINC01534 could promote the abnormal matrix degradation and inflammatory response of OA chondrocytes through the targeted binding of miR-140-5p.

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