ArticleArthritis research & therapy2007
Expression and function of junctional adhesion molecule-C in human and experimental 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 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Vascular Endothelial Barrier in Salivary Glands: From Physiological Regulation to Pathological Impairment of Secretion.International journal of molecular sciences · 2026Review
- Junctional adhesion molecule-C: A multifunctional mediator of cell adhesion.Cellular and molecular life sciences : CMLS · 2025Review
- The Roles of Junctional Adhesion Molecules (JAMs) in Cell Migration.Frontiers in cell and developmental biology · 2022Review
- Article
- Role of Junctional Adhesion Molecule-C in the Regulation of Inner Endothelial Blood-Retinal Barrier Function.Frontiers in cell and developmental biology · 2021Article
- Dynamic trafficking and turnover of JAM-C is essential for endothelial cell migration.PLoS biology · 2019Article
- Targeting junctional adhesion molecule-C ameliorates sepsis-induced acute lung injury by decreasing CXCR4Journal of leukocyte biology · 2018Article
- Divergent JAM-C Expression Accelerates Monocyte-Derived Cell Exit from Atherosclerotic Plaques.PloS one · 2016Article
- The pathogenic role of angiogenesis in rheumatoid arthritis.Angiogenesis · 2015Review
- Platelet-neutrophil interactions under thromboinflammatory conditions.Cellular and molecular life sciences : CMLS · 2015Review
- Rheumatoid arthritis: Microvascular clues to hemiplegia-induced asymmetric RA.Nature reviews. Rheumatology · 2014Article
- Endothelial cell junctional adhesion molecule C plays a key role in the development of tumors in a murine model of ovarian cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- The severity of experimental arthritis is independent of IL-36 receptor signaling.Arthritis research & therapy · 2013Article
- Schwann cell-specific JAM-C-deficient mice reveal novel expression and functions for JAM-C in peripheral nerves.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- The chemokine receptor CXCR2 ligand KC (CXCL1) mediates neutrophil recruitment and is critical for development of experimental Lyme arthritis and carditis.Infection and immunity · 2010Article
- Article
- Article
- Junctional adhesion molecule-C mediates leukocyte infiltration in response to ischemia reperfusion injury.Arteriosclerosis, thrombosis, and vascular biology · 2009Article
- The investigation of synovial genomic targets of bucillamine with microarray technique.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2009Article
- Transcriptional induction of junctional adhesion molecule-C gene expression in activated T cells.Journal of leukocyte biology · 2009Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Junctional adhesion molecule-C (JAM-C) is an adhesion molecule involved in transendothelial migration of leukocytes. In this study, we examined JAM-C expression in the synovium and investigated the role of this molecule in two experimental mouse models of arthritis. JAM-C expression was investigated by reverse transcriptase-polymerase chain reaction and immunohistochemistry. The effects of a monoclonal anti-JAM-C antibody were assessed in antigen-induced arthritis (AIA) and K/BxN serum transfer-induced arthritis. JAM-C was expressed by synovial fibroblasts in the lining layer and associated with vessels in the sublining layer in human and mouse arthritic synovial tissue. In human tissue, JAM-C expression was increased in rheumatoid arthritis (RA) as compared to osteoarthritis synovial samples (12.7 +/- 1.3 arbitrary units in RA versus 3.3 +/- 1.1 in OA; p < 0.05). Treatment of mice with a monoclonal anti-JAM-C antibody decreased the severity of AIA. Neutrophil infiltration into inflamed joints was selectively reduced as compared to T-lymphocyte and macrophage infiltration (0.8 +/- 0.3 arbitrary units in anti-JAM-C-treated versus 2.3 +/- 0.6 in isotype-matched control antibody-treated mice; p < 0.05). Circulating levels of the acute-phase protein serum amyloid A as well as antigen-specific and concanavalin A-induced spleen T-cell responses were significantly decreased in anti-JAM-C antibody-treated mice. In the serum transfer-induced arthritis model, treatment with the anti-JAM-C antibody delayed the onset of arthritis. JAM-C is highly expressed by synovial fibroblasts in RA. Treatment of mice with an anti-JAM-C antibody significantly reduced the severity of AIA and delayed the onset of serum transfer-induced arthritis, suggesting a role for JAM-C in the pathogenesis of arthritis.
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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.