ArticleArthritis research & therapy2005
p53 tumor suppressor gene mutations in fibroblast-like synoviocytes from erosion synovium and non-erosion synovium in rheumatoid arthritis.
Article in Arthritis research & therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- RA-risk synovium exhibits DNA damage coupled with impaired DNA repair in fibroblasts.RMD open · 2026Article
- Function of p53 in angiogenesis and oxidative stress in rheumatoid arthritis.Clinical and experimental medicine · 2025Review
- Iron metabolism in rheumatic diseases.Journal of translational autoimmunity · 2025Review
- Anti-inflammatory effects of PRIMA-1Inflammopharmacology · 2023Article
- Bacterial Compositional Shifts of Gut Microbiomes in Patients with Rheumatoid Arthritis in Association with Disease Activity.Microorganisms · 2022Article
- The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment.Antioxidants (Basel, Switzerland) · 2022Review
- Corticosteroid Treatment-Resistance in Myasthenia Gravis.Frontiers in neurology · 2022Review
- RNA Editing-Associated Post-Transcriptional Gene Regulation in Rheumatoid Arthritis.Bioinformatics and biology insights · 2022Article
- Impact of Posttranslational Modification in Pathogenesis of Rheumatoid Arthritis: Focusing on Citrullination, Carbamylation, and Acetylation.International journal of molecular sciences · 2021Review
- The p53 status in rheumatoid arthritis with focus on fibroblast-like synoviocytes.Immunologic research · 2021Review
- Transformation of fibroblast-like synoviocytes in rheumatoid arthritis; from a friend to foe.Auto- immunity highlights · 2021Review
- Juvenile idiopathic arthritis fibroblast-like synoviocytes influence chondrocytes to alter BMP antagonist expression demonstrating an interaction between the two prominent cell types involved in endochondral bone formation.Pediatric rheumatology online journal · 2020Article
- Restoring synovial homeostasis in rheumatoid arthritis by targeting fibroblast-like synoviocytes.Nature reviews. Rheumatology · 2020Review
- Update on the Pathomechanism, Diagnosis, and Treatment Options for Rheumatoid Arthritis.Cells · 2020Review
- Overexpression of p53 delivered using recombinant NDV induces apoptosis in glioma cells by regulating the apoptotic signaling pathway.Experimental and therapeutic medicine · 2018Article
- SIRT1 promotes tumor-like invasion of fibroblast-like synoviocytes in rheumatoid arthritis via targeting TIMP1.Oncotarget · 2017Article
- Immunomodulatory Function of the Tumor Suppressor p53 in Host Immune Response and the Tumor Microenvironment.International journal of molecular sciences · 2016Review
- The Interactome of the Glucocorticoid Receptor and Its Influence on the Actions of Glucocorticoids in Combatting Inflammatory and Infectious Diseases.Microbiology and molecular biology reviews : MMBR · 2016Review
- TP53 polymorphism may contribute to genetic susceptibility to develop Hashimoto's thyroiditis.Journal of endocrinological investigation · 2015Article
- Perception of self: distinguishing autoimmunity from autoinflammation.Nature reviews. Rheumatology · 2015Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormalities in the p53 tumor suppressor gene have been detected in rheumatoid arthritis (RA) and could contribute to the pathogenesis of chronic disease. To determine whether synoviocytes from invasive synovium in RA have an increased number of mutations compared with non-erosion synoviocytes, p53 cDNA subclones from fibroblast-like synoviocytes (FLS) derived from erosion and non-erosion sites of the same synovium were examined in patients requiring total joint replacement. Ten erosion FLS lines and nine non-erosion FLS lines were established from nine patients with RA. Exons 5-10 from 209 p53 subclones were sequenced (114 from erosion FLS, 95 from non-erosion FLS). Sixty percent of RA FLS cell lines and 8.6% of the p53 subclones isolated from FLS contained p53 mutations. No significant differences were observed between the erosion and non-erosion FLS with regard to the frequency or type of p53 mutation. The majority of the mutations were missense transition mutations, which are characteristic of oxidative damage. In addition, paired intact RA synovium and cultured FLS from the same joints were evaluated for p53 mutations. Matched synovium and cultured synoviocytes contained p53 mutations, although there was no overlap in the specific mutations identified in the paired samples. Clusters of p53 mutations in subclones were detected in some FLS, including one in codon 249, which is a well-recognized 'hot spot' associated with cancer. Our data are consistent with the hypothesis that p53 mutations are randomly induced by genotoxic exposure in small numbers of RA synoviocytes localized to erosion and non-erosion regions of RA synovium. The determining factor for invasiveness might be proximity to bone or cartilage rather than the presence of a p53 mutation.
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