ArticleScientific reports2024
Polydeoxyribonucleotide ameliorates IL-1β-induced impairment of chondrogenic differentiation in human bone marrow-derived mesenchymal stem cells.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The Role of Polydeoxyribonucleotide as a Biotherapy for Musculoskeletal Disorders.International journal of molecular sciences · 2026Review
- Mesenchymal Stem Cell-Inspired Microneedle Platform for NIR-responsive Immunomodulation and Accelerated Chronic Wound Healing.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Article
- Anti-Aging Efficacy of Low-Molecular-Weight Polydeoxyribonucleotide Derived fromInternational journal of molecular sciences · 2025Article
- Thermal-denatured PDRN exhibits increased in vitro pharmacological activities: A functional role of single-stranded DNA random coils.Experimental and therapeutic medicine · 2025Article
- Comparative Analysis of Melatonin and Polydeoxyribonucleotide: Possible Benefits of Co-Treatment Effects and Potential Synergistic Applicability.International journal of molecular sciences · 2025Review
- The Mechanism by Which Estrogen Level Affects Knee Osteoarthritis Pain in Perimenopause and Non-Pharmacological Measures.International journal of molecular sciences · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
Osteoarthritis (OA) is a degenerative disease of the joints, prevalent worldwide. Polydeoxyribonucleotide (PDRN) is used for treating knee OA. However, the role of PDRN in IL-1β-induced inflammatory responses in human bone marrow-derived mesenchymal stem cells (hBMSCs) remains unknown. Here, we investigated the role of PDRN in IL-1β-induced impairment of chondrogenic differentiation in hBMSCs. hBMSCs treated with PDRN showed a large micromass, enhanced safranin O and alcian blue staining intensity, and increased expression of chondrogenic genes in IL-1β-induced inflammatory responses, in addition to regulation of catabolic and anabolic genes. In addition, PDRN treatment suppressed the expression of inflammatory cytokines and mitigated IL-1β-induced apoptosis in hBMSCs. Mechanistically, PDRN treatment increased the formation of cyclic adenosine monophosphate (cAMP) and upregulated the phosphorylation of cAMP-dependent protein kinase A (PKA)/cAMP response element binding protein (CREB) through the adenosine A2A receptor in hBMSCs and thus blocked the nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) signaling pathway. Thus, IL-1β-induced expression of inflammatory cytokines in hBMSCs was directly reduced by adenosine A2A receptor activation. Based on our results, we suggest that PDRN may be a promising MSC-based therapeutic agent for OA.
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