ArticleArthritis research & therapy2007
Morphological characterization of intra-articular HMGB1 expression during the course of collagen-induced arthritis.
Article in Arthritis research & therapy, 2007. 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, 47 citations in OpenAlex.
- Systemic TNF blockade does not modulate synovial expression of the pro-inflammatory mediator HMGB1 in rheumatoid arthritis patients--a prospective clinical study.Arthritis research & therapy · 2008Trial
- Pharmacological intervention of the HMGB1-pCTS-L axis to ameliorate inflammatory diseases.Frontiers in immunology · 2026Review
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- HMGB1 and Toll-like receptors: potential therapeutic targets in autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- High Mobility Group Box 1 (HMGB1): Potential Target in Sepsis-Associated Encephalopathy.Cells · 2023Review
- The Role of HMGB1 in Rheumatic Diseases.Frontiers in immunology · 2022Review
- The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic.Immunity, inflammation and disease · 2021Review
- Sex-Based Differences in Monocytic Lineage Cells Contribute to More Severe Collagen-Induced Arthritis in Female Rats Compared with Male Rats.Inflammation · 2020Article
- The emerging role of fibroblast-like synoviocytes-mediated synovitis in osteoarthritis: An update.Journal of cellular and molecular medicine · 2020Review
- The Role of High-Mobility Group Box-1 and Its Crosstalk with Microbiome in Rheumatoid Arthritis.Mediators of inflammation · 2017Review
- Overexpression of soluble RAGE in mesenchymal stem cells enhances their immunoregulatory potential for cellular therapy in autoimmune arthritis.Scientific reports · 2016Article
- The danger from within: alarmins in arthritis.Nature reviews. Rheumatology · 2016Review
- The role of high-mobility group box protein 1 in collagen antibody-induced arthritis is dependent on vascular endothelial growth factor.Clinical and experimental immunology · 2016Article
- Genomic analysis and differential expression of HMG and S100A family in human arthritis: upregulated expression of chemokines, IL-8 and nitric oxide by HMGB1.DNA and cell biology · 2014Article
- HMGB1: a multifunctional alarmin driving autoimmune and inflammatory disease.Nature reviews. Rheumatology · 2012Review
- High mobility group box protein 1 in complex with lipopolysaccharide or IL-1 promotes an increased inflammatory phenotype in synovial fibroblasts.Arthritis research & therapy · 2011Article
- RAGE and its ligands in bone metabolism.Frontiers in bioscience (Scholar edition) · 2011Review
- Chondrocyte innate immune myeloid differentiation factor 88-dependent signaling drives procatabolic effects of the endogenous Toll-like receptor 2/Toll-like receptor 4 ligands low molecular weight hyaluronan and high mobility group box chromosomal protein 1 in mice.Arthritis and rheumatism · 2010Article
- High-mobility group box protein 1 (HMGB1): an alarmin mediating the pathogenesis of rheumatic disease.Arthritis research & therapy · 2008Review
- Oxaliplatin retains HMGB1 intranuclearly and ameliorates collagen type II-induced arthritis.Arthritis research & therapy · 2008Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group chromosomal box protein 1 (HMGB1) is a structural nuclear protein that promotes inflammation when present extracellularly. Aberrant, extracellular HMGB1 expression has been demonstrated in human and experimental synovitis. The aim of the present study was to elucidate the temporal and spatial expression of HMGB1 compared to that of the central mediators tumor necrosis factor (TNF) and interleukin-1-beta (IL-1beta) during the course of collagen-induced arthritis. Thus, Dark Agouti rats were immunized with homologous type II collagen and synovial tissue specimens were obtained at various time points prior to and during the course of clinical arthritis. Local cytokine responses were assessed by immunohistochemistry and by in situ hybridization. We demonstrate a distinct nuclear expression of HMGB1 at early disease-preceding time points. Preceding clinical onset by a few days, cytoplasmic HMGB1 expression was evident in synoviocytes within the non-proliferative lining layer. Pronounced cytoplasmic and additional extracellular HMGB1 expression coincided with the progression of clinical disease. In advanced arthritis, the number of cells with cytoplasmic HMGB1 expression was quantitatively comparable to that of cells expressing TNF and IL-1beta. Interestingly, although HMGB1 was abundantly expressed throughout the inflamed synovium at a protein level, upregulation of HMGB1 mRNA was restricted mainly to areas of cartilage and bone destruction. In conclusion, these new findings implicate a role for HMGB1 in both inducing and perpetuating inflammatory events of significant importance in the destructive processes in chronic arthritis.
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