ArticleAnnals of the rheumatic diseases2010
Kinetic analysis of synovial signalling and gene expression in animal models of arthritis.
Article in Annals of the rheumatic diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Inflammation-driven bone erosion and reactive remodeling in experimental arthritis revealed by cortical bone surface analysis.Arthritis research & therapy · 2026Article
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- Lacking ARHGAP25 mitigates the symptoms of autoantibody-induced arthritis in mice.Frontiers in immunology · 2023Article
- Pro Nerve Growth Factor and Its Receptor p75NTR Activate Inflammatory Responses in Synovial Fibroblasts: A Novel Targetable Mechanism in Arthritis.Frontiers in immunology · 2022Article
- Activation of c-Jun N-Terminal Kinase, a Potential Therapeutic Target in Autoimmune Arthritis.Cells · 2020Review
- Evaluation of the therapeutic potential of the selective p38 MAPK inhibitor Skepinone-L and the dual p38/JNK 3 inhibitor LN 950 in experimental K/BxN serum transfer arthritis.Inflammopharmacology · 2019Article
- Capsaicin-sensitive sensory nerves exert complex regulatory functions in the serum-transfer mouse model of autoimmune arthritis.Brain, behavior, and immunity · 2015Article
- Activated protein C inhibits proliferation and tumor necrosis factor α-stimulated activation of p38, c-Jun NH2-terminal kinase (JNK) and Akt in rheumatoid synovial fibroblasts.Molecular medicine (Cambridge, Mass.) · 2013Article
- Pre-rheumatoid arthritis: predisposition and transition to clinical synovitis.Nature reviews. Rheumatology · 2012Review
- Selective involvement of ERK and JNK mitogen-activated protein kinases in early rheumatoid arthritis (1987 ACR criteria compared to 2010 ACR/EULAR criteria): a prospective study aimed at identification of diagnostic and prognostic biomarkers as well as therapeutic targets.Annals of the rheumatic diseases · 2012Article
- Regulation of inflammatory arthritis by the upstream kinase mitogen activated protein kinase kinase 7 in the c-Jun N-terminal kinase pathway.Arthritis research & therapy · 2012Article
- c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases.The open rheumatology journal · 2012Article
- Suppression of collagen-induced arthritis in growth arrest and DNA damage-inducible protein 45β-deficient mice.Arthritis and rheumatism · 2011Article
- "Go upstream, young man": lessons learned from the p38 saga.Annals of the rheumatic diseases · 2010Review
- 'Rac'-ing upstream to treat rheumatoid arthritis.Arthritis research & therapy · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAnimal models of arthritis are frequently used to evaluate novel therapeutic agents. However, their ability to predict responses in humans is variable.
objectiveTo examine the time course of signalling molecule and gene expression in two models of arthritis to assist with selection of the model and timing of drug administration.
methodsThe passive K/BxN serum transfer and collagen-induced arthritis (CIA) models were studied. Activation of MAP kinase and interferon (IFN)-response pathways was evaluated by quantitative PCR and western blot analysis of ankle joints at various time points during the models.
resultsThe kinetics of gene expression and kinase phosphorylation were strikingly different in passive K/BxN and CIA. All three MAP kinases (ERK, JNK and p38) and upstream kinases were activated within days in passive K/BxN and declined as arthritis severity decreased. Surprisingly, IFN-regulated genes, including IRF7, were not induced in the model. In CIA, activation of ERK and JNK was surprisingly low and p38 phosphorylation mainly peaked late in the disease. IFN-response genes were activated during CIA, with especially prominent peaks at the onset of clinical arthritis.
conclusionsTiming of treatment and selection of CIA or passive K/BxN might have an important impact on therapeutic response. p38, in particular, increases during the late stages of CIA. ERK and JNK patterns are similar in passive K/BxN and rheumatoid arthritis (RA), while IFN-response genes in CIA and RA are similar. The dichotomy between RA and animal models could help explain the poor correlation between efficacy in RA and preclinical studies.
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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.