ArticleMolecular medicine reports2019
lncRNA‑NR024118 overexpression reverses LPS‑induced inflammatory injury and apoptosis via NF‑κB/Nrf2 signaling in ATDC5 chondrocytes.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- Application of 3D bioprinting technology apply to assessing Dangguiniantongtang (DGNT) decoctions in arthritis.Chinese medicine · 2024Article
- Intervertebral disc degeneration and osteoarthritis: a common molecular disease spectrum.Nature reviews. Rheumatology · 2023Review
- Long noncoding RNAs in mesenchymal stromal/stem cells osteogenic differentiation: Implications in osteoarthritis pathogenesis.World journal of stem cells · 2022Article
- Fxyd5 activates the NF‑κB pathway and is involved in chondrocytes inflammation and extracellular matrix degradation.Molecular medicine reports · 2022Article
- LncRNA NR024118 is downregulated in sepsis and inhibits LPS‑induced apoptosis of cardiomyocytes.Molecular medicine reports · 2021Article
- Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
- The Emerging Role of Non-Coding RNAs in Osteoarthritis.Frontiers in immunology · 2021Review
- Purified Sika deer antler protein attenuates GM-induced nephrotoxicity by activating Nrf2 pathway and inhibiting NF-κB pathway.Scientific reports · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is one of the most prevalent types of chronic joint diseases. Chondrocytes survival is closely associated with the destruction of joints in patients with OA. Long noncoding RNAs (lncRNAs) serve a critical role in OA. However, to the best of our knowledge, the role of lncRNAs NR024118 in OA has not been examined. In the present study, the expression levels of NR024118 in lipopolysaccharide (LPS)‑induced chondrocytes was measured using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and the apoptosis levels of cells was determined using flow cytometry. The levels of scavenged reactive oxygen species and expression levels of the antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and heme oxygenase‑1 (HO‑1) were measured using specialized detection kits. The expression of interleukin (IL)‑1β, IL‑6 and IL‑18 were measured using ELISA. Expression of the cell apoptosis markers Bcl‑2, Bax, Bcl‑2‑like protein 11, NF‑κB, phosphorylated (p)‑NF‑κB inhibitor β (IκBβ), IκBβ, p‑transcription factor p65 (p65) and p65, and nuclear factor erythroid‑2 related factor 2 (Nrf2) signaling pathways‑associated proteins, Nrf2, HO‑1 and quinone oxidoreductase‑1 were detected by western blot analysis and RT‑qPCR. The results indicated that in ATDC5 cells, apoptosis, oxidative stress and inflammation were significantly increased and the expression level of NR024118 was significantly decreased by LPS‑mediated induction. NR024118 overexpression significantly reversed the effects of LPS treatment in the ATDC5 cell line. In addition, the overexpression of NR024118 decreased NF‑κB expression levels and activated the Nrf2 signaling pathways in LPS‑induced ATDC5 cells. The present study demonstrated that NR024118 attenuated the effects of LPS‑induction on ATDC5 cells. These results suggest that NR024118 may be a potential target for diagnosis and treatment of OA.
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