ArticleRheumatology (Oxford, England)2011
Advanced glycation end products induce the expression of interleukin-6 and interleukin-8 by receptor for advanced glycation end product-mediated activation of mitogen-activated protein kinases and nuclear factor-κB in human osteoarthritis chondrocytes.
Article in Rheumatology (Oxford, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 184 citations in OpenAlex.
- Increased expression of damage-associated molecular patterns (DAMPs) in osteoarthritis of human knee joint compared to hip joint.Molecular and cellular biochemistry · 2017Trial
- Serum pentosidine concentration is associated with radiographic severity of lumbar spondylosis in a general Japanese population.Journal of bone and mineral metabolism · 2017Trial
- The Effect of Physical, Biochemical, and Electrical Culture Conditions on Articular Chondrocytes Used for Cartilage Tissue Engineering: A Narrative Review.International journal of molecular sciences · 2026Review
- Unraveling mortality risk in pediatric acute respiratory distress syndrome: key biomarkers and pathophysiological insights.Pediatric research · 2026Review
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- High-mobility Group Protein 1/ Receptor for Advanced Glycation End Products/ Nuclear Factor-κB Signalling Pathway Contributes to the Pathogenic Process of Striatal Neuron Impairment in the Rat Model of Parkinson's Disease.Brain and behavior · 2026Article
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Association between knee stiffness and MRI-detected lesions: data from the osteoarthritis initiative (OAI).BMC musculoskeletal disorders · 2025Article
- Soluble receptor for advanced glycation end products and diabetes in Black and White Americans: the REGARDS Study.Obesity medicine · 2025Article
- Correlation between serum advanced glycation end-products and their receptor-mediated oxidative stress and perinatal outcomes in gestational diabetes mellitus.World journal of diabetes · 2025Article
- Inflammatory mechanisms underlying metabolic syndrome-associated and potential treatments.Osteoarthritis and cartilage open · 2025Article
- Metabolic Reprogramming in Stromal and Immune Cells in Rheumatoid Arthritis and Osteoarthritis: Therapeutic Possibilities.European journal of immunology · 2025Review
- Effect of diabetes mellitus on physical function in patients with osteoarthritis: a cross-sectional observational study.Frontiers in endocrinology · 2025Observational
- Albumin does not induce IL-6 release and toll-like receptor activation in vitro: Role of endotoxin contamination and biochemical modifications.BBA advances · 2025Article
- Emerging therapeutic potential of glucagon-like Peptide-1 receptor agonists in knee osteoarthritis: a systematic review.Frontiers in pharmacology · 2025Review
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Mechanisms of AGE-induced VSMC phenotypic switching and macrophage modulation in human abdominal aortic aneurysms.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- The role of metabolites in the progression of osteoarthritis: Mechanisms and advances in therapy.Journal of orthopaedic translation · 2025Review
- NFκB and JNK pathways mediate metabolic adaptation upon ESCRT-I deficiency.Cellular and molecular life sciences : CMLS · 2024Article
- Novel perspectives on leptin in osteoarthritis: Focus on aging.Genes & diseases · 2024Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo investigate whether advanced glycation end products (AGEs) induce the expression of IL-6 and IL-8 through the receptor for AGEs (RAGE)-activated pathways in human OA chondrocytes.
methodsOA chondrocytes were stimulated with AGE-modified BSA (AGE-BSA). Gene expression of IL-6 and IL-8 was quantified by TaqMan assays and the production was determined using ELISAs. Immunoblotting was used to analyse the activation of mitogen-activated protein kinases (MAPKs) and the degradation of IκBα. Activation of NF-κB was determined using an ELISA. Pharmacological studies to elucidate the involved pathways were executed using transfection with small interfering RNAs (siRNAs), inhibitors of MAPKs and NF-κB.
resultsAGE-BSA induced the expression of IL-6 and IL-8 in OA chondrocytes, which was inhibited by pre-treatment with soluble RAGE (sRAGE) or RAGE knockdown by siRNAs. Treatment with SB202190 (p38-MAPK inhibitor) or PD98059 (ERK inhibitor) inhibited AGE-BSA-induced IL-6 and IL-8 expression. However, SP600125 (JNK inhibitor) had no effect on AGE-BSA-induced IL-6 expression but inhibited the expression of IL-8. Treatment with NF-κB inhibitors suppressed AGE-BSA-induced IL-6 and IL-8 expression.
conclusionsThis is the first study to demonstrate that AGEs induce the expression of IL-6 and IL-8 in OA chondrocytes. A novel finding of our studies is that in OA chondrocytes, AGE-BSA-induced expression of IL-6, but not of IL-8, was independent of the JNK pathway. Activation of NF-κB was an absolute requirement for both IL-6 and IL-8 expression. These results demonstrate that AGE-BSA-induced expression of IL-6 and IL-8 via RAGE is mediated through different MAPK signalling pathways in OA and possibly in other degenerative diseases.
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Registered trials
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 OpenQuestion graph.