ArticleMolecular medicine reports2017
Reduced miR‑26a and miR‑26b expression contributes to the pathogenesis of osteoarthritis via the promotion of p65 translocation.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- Review
- An Integrated Machine Learning Framework for Developing and Validating a Diagnostic Model of Hub Genes Related to Lipid Metabolism in Chronic Rhinosinusitis.Journal of inflammation research · 2025Article
- Platelet-rich plasma alleviates knee arthritis in rats by inhibiting p65.Cell and tissue banking · 2024Article
- CircRNA SEC24A promotes osteoarthritis through miR-107-5p/CASP3 axis.Regenerative therapy · 2024Article
- MicroRNA-138: an emerging regulator of skeletal development, homeostasis, and disease.American journal of physiology. Cell physiology · 2023Review
- MicroRNA Modulation during Orthodontic Tooth Movement: A Promising Strategy for Novel Diagnostic and Personalized Therapeutic Interventions.International journal of molecular sciences · 2022Review
- Characterization of microRNA Levels in Synovial Fluid from Knee Osteoarthritis and Anterior Cruciate Ligament Tears.Biomedicines · 2022Article
- Dysregulated microRNA expression in rheumatoid arthritis families-a comparison between rheumatoid arthritis patients, their first-degree relatives, and healthy controls.Clinical rheumatology · 2021Article
- Role of microRNA Shuttled in Small Extracellular Vesicles Derived From Mesenchymal Stem/Stromal Cells for Osteoarticular Disease Treatment.Frontiers in immunology · 2021Review
- Astilbin prevents osteoarthritis development through the TLR4/MD-2 pathway.Journal of cellular and molecular medicine · 2020Article
- MIR-140-5p affects chondrocyte proliferation, apoptosis, and inflammation by targeting HMGB1 in osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Epigenetics in osteoarthritis: Novel spotlight.Journal of cellular physiology · 2019Review
- Review
- MicroRNA-26a reduces synovial inflammation and cartilage injury in osteoarthritis of knee joints through impairing the NF-κB signaling pathway.Bioscience reports · 2019Article
- Scaffold-Based Gene Therapeutics for Osteochondral Tissue Engineering.Frontiers in pharmacology · 2019Review
- Hyaluronic Acid: Molecular Mechanisms and Therapeutic Trajectory.Frontiers in veterinary science · 2019Review
- Onset and Progression of Human Osteoarthritis-Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?International journal of molecular sciences · 2018Review
- MicroRNAs and Osteoarthritis.Cells · 2018Review
- The Involvement of MicroRNAs in Osteoarthritis and Recent Developments: A Narrative Review.Mediterranean journal of rheumatology · 2018Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a common chronic joint disease, the etiology of which is complex. Disturbance to proinflammatory and anti‑inflammatory signaling pathways is a major cause of OA. MicroRNAs (miRNAs/miR) are a group of endogenous, short, non‑coding RNAs, the expression profile of which is disturbed in the cartilage of patients with OA. To determine the function of miRNAs during the progression of OA, the present study detected the expression levels of nine candidate miRNAs in cartilage samples from 33 patients with OA. The results demonstrated that miR‑26a, miR‑26b, miR‑138 and miR‑140 were downregulated in patients with OA. As predicted by a bioinformatics analysis and confirmed by luciferase assay and western blotting, the present study revealed that miR‑26a and miR‑26b are able to suppress karyopherin subunit alpha 3 (KPNA3) expression by targeting its 3'‑untranslated region. Since KPNA3 is an important mediator that modulates nuclear factor (NF)‑κB p65 translocation, the present study examined the impact of miR‑26a and miR‑26b on NF‑κB signaling. The results indicated that transfection of cells with a miR‑26a or miR‑26b inhibitor may promote NF‑κB p65 translocation from the cytoplasm to the nucleus via the upregulation of KPNA3. Furthermore, the expression levels of matrix metalloproteinase‑3, ‑9, ‑13 and cyclooxygenase‑2 were upregulated following transfection with a miR‑26a or miR‑26b inhibitor. These results indicate that downregulation of miR‑26a and miR‑26b may contribute to the pathogenesis of OA via promotion of the NF‑κB signaling pathway. The present study sheds light on the pathogenesis of OA and may provide a target for the development of therapeutic methods for the treatment of OA.
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