Inhibition of sterol regulatory element-binding protein-2 alleviates high-fat diet-induced deterioration of knee cartilage: an osteoarthritis animal model study

Tao, Ke; Li, R.; Li, H.; Ke, Yan; Lin, Jianhao

doi:10.1016/j.joca.2019.02.373

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“…In the process of the development of OA, abnormal metabolic dysfunction occurs in chondrocytes, and the synthesis of aggrecan and collagen II, the main components of chondrocyte extracellular matrix, are inhibited, while the synthesis of MMPs is increased, thus promoting the abnormal degradation of chondrocyte extracellular matrix. 30-32 In addition, the large release of inflammatory factors such as IL-1β, IL-6, NO, PGE2, and TNF-α not only damages chondrocytes but also induces extracellular matrix degradation, which is also an important reason for promoting the development of OA. 33-35 In this study, it was found that silencing LINC01534 alleviated the inhibitory effect of IL-1β on the major components of chondrocytes and significantly inhibited the synthesis of MMP-3, MMP-9, and MMP-13, while miR-140-5p inhibitor reversed this effect.…”

Section: Discussionmentioning

confidence: 99%

LINC01534 Promotes the Aberrant Metabolic Dysfunction and Inflammation in IL-1β-Simulated Osteoarthritic Chondrocytes by Targeting miR-140-5p

Wei

Wang

et al. 2019

CARTILAGE

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Objective 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 in OA chondrocytes induced by interleukin-1β (IL-1β). Methods The quantitative real-time polymerase chain reaction (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 expressions of aggrecan and collagen II in the chondrocyte were detected by Western blot. The levels of tumor necrosis factor–α (TNF-α), IL-8, IL-6, MMP-13, MMP-9, MMP-3, and prostaglandin E2 (PGE2) in chondrocyte were determined by enzyme-linked immunosorbernt assay. Bioinformatics, dual luciferin gene reporting, RNA pulldown, and Northern blot were used to determine the interaction between LINC01534 and miR-140-5p. Results The results showed that LINC01534 was upregulated 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 downregulated the expression of matrix metalloproteinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also significantly inhibited the productions of proinflammatory factors NO, PGE2, TNF-α, IL-6, and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was confirmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion Therefore, 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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