ArticleExperimental and therapeutic medicine2021
LINC00473 exacerbates osteoarthritis development by promoting chondrocyte apoptosis and proinflammatory cytokine production through the miR-424-5p/LY6E axis.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of Key Glycolysis-Related Genes in Osteoarthritis and Their Correlation with Immune Infiltration Using Bioinformatics Analysis and Machine Learning.Open access rheumatology : research and reviews · 2025Article
- Circular RNA KIAA0564 Serves as a Competitive Endogenous RNA for MicroRNA-424-5p, Mediating the Expression of Lysine Demethylase 4a, Thereby Facilitating Intervertebral Disc Degeneration.Applied biochemistry and biotechnology · 2024Article
- microRNA-105-5p protects against chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression by targeting SPARCL1.Histology and histopathology · 2024Article
- Advances in Research on the Regulatory Roles of lncRNAs in Osteoarthritic Cartilage.Biomolecules · 2023Review
- The emerging role of lncRNAs in osteoarthritis development and potential therapy.Frontiers in genetics · 2023Review
- Blood RNA Sequencing Indicates UpregulatedInternational journal of molecular sciences · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a common degenerative joint disease that has been identified as one of the major health burdens in aging individuals. Long non-coding RNAs (lncRNAs) participate in the development of diverse diseases, including OA. Among them, lncRNA long intergenic non-protein coding RNA 473 (LINC00473) is one of the few upregulated lncRNAs. The present study aimed to explore the role of LINC00473 and its regulatory mechanism in OA development. Flow cytometry analyses and ELISA were carried out to detect chondrocyte apoptosis and the concentration of proinflammatory cytokines, respectively. The results suggested that LINC00473 knockdown significantly reduced chondrocyte apoptosis and the production of proinflammatory cytokines in IL-1β-stimulated C28/I2 cells compared with transfection with small interfering RNA-negative control (si-NC). Western blot analyses were performed to examine protein levels of apoptotic markers (caspase-3, Bax and Bcl-2) in C28/I2 cells. Subsequently, an OA rat model was established to explore the role of LINC00473
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