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Current Pharmaceutical Design

Author(s): Lisong Li*, Lianfang Zhang*, Yong Zhang*, Dinghua Jiang, Wu Xu, Haiyue Zhao and Lixin Huang

DOI: 10.2174/1381612825666190801141801

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Inhibition of Long Non-coding RNA CTD-2574D22.4 Alleviates LPS-induced Apoptosis and Inflammatory Injury of Chondrocytes

Page: [2969 - 2974] Pages: 6

  • * (Excluding Mailing and Handling)

Abstract

Background: Osteoarthritis (OA) is a common joint disease characterized by cartilage degeneration. Long non-coding RNAs (lncRNAs) have been associated with inflammatory diseases, including OA. Here, we investigated the potential molecular role of lncRNAs in OA pathogenesis.

Methods: ATDC5 cells were treated with lipopolysaccharides (LPS), and qPCR was used to identify and determine expression of potential lncRNAs involved in LPS-induced chondrocyte injury. Cell viability, apoptosis, and expression of cartilage-related genes and inflammatory cytokines were assessed after CTD-2574D22.4 knockdown.

Results: After LPS stimulation, CTD-2574D22.4 was found to be the second highest up-regulated gene, and the enhanced expression was validated in OA chondrocytes. Moreover, CTD-2574D22.4 inhibition significantly rescued cell viability, suppressed by LPS stress, and markedly attenuated LPS-induced apoptosis. The expression of cartilage-degrading enzymes MMP-13 and ADAMTS-5 were increased, while type II collagen was reduced after LPS treatment. This trend was largely reversed by CTD-2574D22.4 knockdown. Additionally, mRNA and protein levels of key inflammatory cytokines (TNF-a, IL-6, and IL-1β) were significantly elevated in the LPS group and partially relieved upon CTD-2574D22.4 knockdown.

Conclusion: CTD2574D22.4 knockdown ameliorates LPS-induced cartilage injury by protecting chondrocytes from apoptosis via anti-inflammation and anti- cartilage-degrading pathways. Thus, CTD2574D22.4 might be a potential diagnostic and therapeutic target for OA.

Keywords: Osteoarthritis, LncRNA, CTD-2574D22.4, apoptosis, inflammatory injury, cartilage degeneration.

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