ArticleArthritis research & therapy2020
PRMT5 inhibition attenuates cartilage degradation by reducing MAPK and NF-κB signaling.
Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Self-Assembled Hydrogels: A Novel Drug Delivery System for Osteoarthritis.Current issues in molecular biology · 2026Review
- Exploring the mechanism of action of astragaloside in the treatment of osteoarthritis based on network pharmacology.Biomedical engineering online · 2025Article
- Article
- PRMT5 inhibition reduces hyperinflammation in a murine model of secondary hemophagocytic lymphohistiocytosis.Blood advances · 2025Article
- Landscape of Histone Posttranslational Modifications in Osteoarthritis.Journal of inflammation research · 2025Review
- Knockdown of DAPK1 inhibits IL-1β-induced inflammation and cartilage degradation in human chondrocytes by modulating the PEDF-mediated NF-κB and NLRP3 inflammasome pathway.Innate immunity · 2024Article
- PRMT5 participates in B cell overactivation in patients with primary Sjogren's syndrome (pSS) through RSAD2-mediated NF-κB signaling.Immunity, inflammation and disease · 2023Article
- PRMT5 inhibition ameliorates inflammation and promotes the osteogenic differentiation of LPS‑induced periodontal stem cells via STAT3/NF‑κB signaling.Experimental and therapeutic medicine · 2023Article
- The epigenetic players and the chromatin marks involved in the articular cartilage during osteoarthritis.Frontiers in physiology · 2023Review
- Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression.Frontiers in immunology · 2023Review
- The circSPON2/miR-331-3p axis regulates PRMT5, an epigenetic regulator of CAMK2N1 transcription and prostate cancer progression.Molecular cancer · 2022Article
- Effect of condylar chondrocyte exosomes on condylar cartilage osteogenesis in rats under tensile stress.Frontiers in bioengineering and biotechnology · 2022Article
- The Influence of Arginine Methylation in Immunity and Inflammation.Journal of inflammation research · 2022Review
- Splicing alterations in healthy aging and disease.Wiley interdisciplinary reviews. RNA · 2021Review
- Review
- Protein Arginine Methyltransferase 5 FunctionsFrontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesA role for the type II arginine methyltransferase PRMT5 in various human diseases has been identified. In this study, the potential mechanism underlying the involvement of PRMT5 in the pathological process leading to osteoarthritis (OA) was investigated.
methodsPRMT5 expression in cartilage tissues from patients with OA and control individuals was assessed by immunohistochemical staining. The regulatory and functional roles of PRMT5 in the chondrocytes of patients with OA and control individuals were determined by western blotting and reverse transcription polymerase chain reaction. The effects of the PRMT5 inhibitor EPZ on interleukin-1β-induced inflammation were examined in the chondrocytes of patients with OA and in the destabilized medial meniscus (DMM) of a mouse model of OA.
resultsPRMT5 was specifically upregulated in the cartilage of patients with OA. Moreover, adenovirus-mediated overexpression of PRMT5 in human chondrocytes caused cartilage degeneration. This degeneration was induced by elevated expression levels of matrix-degrading enzymes (matrix metalloproteinase-3 (MMP-3) and matrix metalloproteinase-13 (MMP-13)) in chondrocytes. The activation of the MAPK and nuclear factor κB signaling pathways was evidenced by elevated levels of p-p65, p-p38, and p-JNK. These effects were attenuated by inhibiting the expression of PRMT5. In the mouse model, EPZ inhibited PRMT5 expression, thus protecting mouse cartilage from DMM-induced OA.
conclusionsOur results demonstrate that PRMT5 is a crucial regulator of OA pathogenesis, implying that EPZ has therapeutic value in the treatment of this cartilage-destroying disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.