ArticleJournal of inflammation research2025
LncRNA NONHSAT248596.1 Promotes Osteoarthritis via miR-146a-5p/CXCR4 Axis by Inducing Chondrocyte Apoptosis and Extracellular Matrix Degradation.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Osteoarthritis (OA) is characterized by articular cartilage degeneration, osteophyte formation, subchondral bone remodeling, synovitis, and joint capsule fibrosis, yet its underlying molecular mechanisms and the functional roles of long non-coding RNAs (lncRNAs) remain poorly understood. This study aimed to investigate the role of lncRNA NONHSAT248596.1 in the pathogenesis of OA through the miR-146a-5p/CXCR4 axis. Materials and Methods: The experimental systems included human articular cartilage samples, a rabbit model of OA, and chondrocytes treated with 100 ng/mL SDF-1. DIANA software predicted lncRNAs targeting the miR-146a-5p/CXCR4 axis. Dual-luciferase reporter assay verified the molecular interactions. The expression levels of target genes and proteins (CXCR4, miR-146a-5p, NONHSAT248596.1, TNF-α, IL-1β, MMP-13, collagen II, and aggrecan) were analyzed using qRT-PCR, Western blotting, and ELISA both in vitro and in vivo. Cell viability and apoptosis were measured by CCK-8 assay and flow cytometry, respectively. Cartilage pathology in the rabbit models was assessed via safranin O and hematoxylin and eosin staining at 4, 8, and 12 weeks. Results: LncRNA NONHSAT248596.1 was significantly upregulated in OA patients and in SDF-1-induced chondrocytes. The dual-luciferase assays confirmed that NONHSAT248596.1 interacted with miR-146a-5p, and miR-146a-5p interacted with CXCR4 in OA. Overexpression of NONHSAT248596.1 promoted chondrocyte apoptosis (p Conclusion: LncRNA NONHSAT248596.1 promotes OA via miR-146a-5p/CXCR4 axis by inducing chondrocyte apoptosis and extracellular matrix degradation. These results identify NONHSAT248596.1 as a potential therapeutic target for OA intervention and underscore the miR-146a-5p/CXCR4 axis as a critical regulatory pathway for cartilage protection.
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