ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022
RPL38 knockdown inhibits the inflammation and apoptosis in chondrocytes through regulating METTL3-mediated SOCS2 m6A modification in osteoarthritis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- IGF2BP3 Overexpression Accelerates Osteoarthritis Progression by Promoting Glycolysis via mThe Kaohsiung journal of medical sciences · 2026Article
- METTL3 promotes chondrocyte injury in osteoarthritis by increasing CTSB expression.Journal of orthopaedic surgery and research · 2025Article
- Identification of energy metabolism and m6A-related gene clusters in Kashin-Beck disease based on bioinformatics analysis.BMC musculoskeletal disorders · 2025Article
- RNA Modifications in Osteoarthritis: Epitranscriptomic Insights into Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2025Review
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- Methyltransferase-Like 3-Mediated NJournal of cellular and molecular medicine · 2025Review
- Mechanistic and therapeutic insights into the function of N6-methyladenosine in arthritic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Epigenetics and Herbs: Potential Therapeutic Strategies for Osteoarthritis of the Knee.Journal of pain research · 2025Review
- Novel Insights into the Regulatory Role of N6-Methyladenosine in the Pathogenesis and Clinical Treatment of Osteoarthritis: Research Status and Prospect.Journal of inflammation research · 2025Review
- Key Role of STAT3 in Osteoarthritis: From Pathogenic Mechanisms to Targeted Therapy.International journal of nanomedicine · 2025Review
- Review
- RpL38 modulates germ cell differentiation by controlling Bam expression in Drosophila testis.Science China. Life sciences · 2024Article
- Anandamide Modulates Thermal Avoidance in Caenorhabditis elegans Through Vanilloid and Cannabinoid Receptor Interplay.Neurochemical research · 2024Article
- Desflurane alleviates LPS-induced acute lung injury by modulating let-7b-5p/HOXA9 axis.Immunologic research · 2024Article
- RPL35 downregulated by mechanical overloading promotes chondrocyte senescence and osteoarthritis development via Hedgehog-Gli1 signaling.Journal of orthopaedic translation · 2024Article
- Recent advances of m6A methylation in skeletal system disease.Journal of translational medicine · 2024Review
- N6-Methyladenosine in Cell-Fate Determination of BMSCs: From Mechanism to Applications.Research (Washington, D.C.) · 2024Article
- siRNA therapy in osteoarthritis: targeting cellular pathways for advanced treatment approaches.Frontiers in immunology · 2024Review
- Overview of distinct N6-Methyladenosine profiles of messenger RNA in osteoarthritis.Frontiers in genetics · 2023Article
- Emerging role of METTL3 in inflammatory diseases: mechanisms and therapeutic applications.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRibosomal protein L38 (RPL38) was found upregulated in osteoarthritic peripheral blood mononuclear cells, however, its role in progression of osteoarthritis has not been characterized.
methodsThe protein levels of RPL38 and SOCS2 in cartilage tissues from OA patients and controls were detected with Western blotting. IL-1β was used to stimulate primary chondrocytes to establish an OA cell model, and RPL38 siRNA (si-RPL38) was transfected into chondrocytes to investigate the effect of RPL38 knockdown on cell viability, apoptosis, inflammatory factor secretion and extracellular matrix degradation. Then, the mechanism that RPL38 regulate the SOCS2 expression and SOCS2-induced chondrocyte dysfunction was explored. The methyltransferase-like 3 (METTL3)-mediated m6A modification of SOCS2 mRNA was confirmed, and the interaction of RPL38 and METTL3 was verified. Moreover, the effects of SOCS2 overexpression on IL-1β-induced chondrocyte dysfunction and SOCS2 knockdown on the restoration of chondrocyte function by siRPL38 were investigated. Finally, RPL38 was knocked down in vivo and its role in OA progression was validated.
resultsRPL38 was upregulated and SOCS2 was downregulated in OA cartilages. RPL38 knockdown or SOCS2 overexpression either attenuated IL-1β-induced chondrocyte apoptosis, inflammatory cytokine secretion, and ECM degradation. RPL38 directly interacted with METTL3 and it inhibited SOCS2 expression through METTL3-mediated m6A modification. SOCS2 knockdown activated the JAK2/STAT3 proinflammatory pathway and reversed the effects of RPL38 knockdown on IL-1β-induced chondrocyte apoptosis, inflammation and ECM degradation. RPL38 knockdown alleviated cartilage tissue damage and ECM degradation in OA mice.
conclusionRPL38 knockdown inhibited osteoarthritic chondrocyte dysfunction and alleviated OA progression through promoting METTL3-m6A-mediated SOCS2 expression.
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