Induction of a CXCL8 binding site on endothelial syndecan‐3 in rheumatoid synovium

Patterson, Angela; Gardner, Lucy; Shaw, Joseph W.; Gourichon, David; Loreau, Emilie; Aguilar, Luc; Ashton, Brian A.; Middleton, Jim

doi:10.1002/art.21222

Cited by 42 publications

(53 citation statements)

References 73 publications

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“…The method of Roskams et al 38 was followed, using the anti-syndecan and anti-glypican-1 antibodies, with minor modifications; for glypican-3 the method of Patterson et al 14 for polyclonal antibodies was used with minor modifications, for glypican-4 the polyclonal antibody was diluted in 10% human serum and detected with swine anti-rabbit horse radish peroxidase conjugate diluted in 10% human serum. Briefly, 10 μm thick serial cryostat sections of synovia and skin were dried for 1 h and stored at −80°C until required.…”

Section: Methodsmentioning

confidence: 99%

“…Using animal knockout models and isolated cells, syndecan-1 and syndecan-4 have been shown to be involved in regulating inflammatory responses,19 binding chemokines20 21 and forming chemokine gradients 22 23. The chemokine CXCL8 has been shown to bind to syndecan-2 in cultured human umbilical vein endothelial cells24 and we recently showed the induction of a CXCL8 binding site on syndecan-3 in the endothelial cells of the RA synovium 14. However, little is known about the expression of syndecans and glypicans by the various cell types of the chronically inflamed synovium, although other proteoglycans bearing GAGs such as dermatan sulphate have been identified in this tissue 25.…”

mentioning

confidence: 95%

“…Syndecan-3 was first identified on neuronal cells and has been associated with the generation of cerebellar fibrillar plaques in Alzheimer disease 10. It is also an HSPG of the musculoskeletal system 11 – 14. Glypicans are widely expressed in embryonic and adult tissues such as ovary, intestine and central nervous system, and are involved in growth factor signalling 15.…”

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confidence: 99%

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Differential expression of syndecans and glypicans in chronically inflamed synovium

Patterson

Cartwright

Gourichon

et al. 2007

Annals of the Rheumatic Diseases

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Background:Membrane-bound heparan sulphate proteoglycans (HSPGs) act as co-receptors and presenters of cytokines and are involved in cell–matrix and cell–cell adhesion.Aim:To investigate which HSPGs are expressed in knee joint synovia from patients with different forms of arthritis and normal individuals.Methods:Synovial samples were obtained from patients with early rheumatoid arthritis (n = 8), longstanding rheumatoid arthritis (n = 13), psoriatic arthritis (n = 7), osteoarthritis (n = 6) and normal joints (n = 12). Expression of syndecan-1, -2, -3 and -4 and glypican-1, -3 and -4 was analysed by immunohistochemistry and dual label immunofluorescence.Results:The expression of HSPGs in chronically inflamed synovium exhibited a differential distribution. Syndecan-1 was present in the mononuclear infiltrates of synovia from patients with rheumatoid and psoriatic arthritis where it was expressed by plasma cells. Syndecan-2 was present mainly in blood vessels where it occurred on endothelial cells, pericytes and smooth muscle cells. Syndecan-3 stained intensely in endothelial cells but also occurred in sublining macrophages and the lining layer. Glypican-4 occurred in the lining layer and blood vessels. Increased expression of these HSPGs was apparent in rheumatoid and psoriatic compared to osteoarthritic and normal synovia. Little or no staining for syndecan-4, glypican-1 and glypican-3 was seen in all samples.Discussion:Selected HSPGs, such as syndecan-1, -2 and -3 and glypican-4, could play a part in the pathophysiology of arthritis, such as the migration and retention of leukocytes and angiogenesis in the chronically inflamed synovium.

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Section: Methodsmentioning

confidence: 99%

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Differential expression of syndecans and glypicans in chronically inflamed synovium

Patterson

Cartwright

Gourichon

et al. 2007

Annals of the Rheumatic Diseases

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“…The sections were blocked in 5% goat serum and incubated overnight at 4°C with IL-33 Nter rabbit polyclonal antibody ( Semiquantitative RT-PCR. Isolation of microvascular ECs from the different tissues and RNA analysis by semiquantitative RT-PCR was performed as described (34,36) with the following primer pairs: 5Ј-CACCCCTCAAATGAATCAGG-3Ј and 5Ј-GGAGCTCCA-CAGAGTGTTCC-3Ј for IL-33, 5Ј-ACCACAGTCCATGCCAT-CAC-3Ј and 5Ј-TCCACCACCCTGTTGCTGTA-3Ј for the internal control GAPDH.…”

Section: Methodsmentioning

confidence: 99%

IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factorin vivo

Carrière

Roussel

Ortéga

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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875

869

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Recent studies indicate that IL-1␣ functions intracellularly in pathways independent of its cell surface receptors by translocating to the nucleus and regulating transcription. Similarly, the chromatinassociated protein HMGB1 acts as both a nuclear factor and a secreted proinflammatory cytokine. Here, we show that IL-33, an IL-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines, is an endothelium-derived, chromatin-associated nuclear factor with transcriptional repressor properties. We found that IL-33 is identical to NF-HEV, a nuclear factor preferentially expressed in high endothelial venules (HEV), that we previously characterized. Accordingly, in situ hybridization demonstrated that endothelial cells constitute a major source of IL-33 mRNA in chronically inflamed tissues from patients with rheumatoid arthritis and Crohn's disease. Immunostaining with three distinct antisera, directed against the N-terminal part and IL-1-like C-terminal domain, revealed that IL-33 is a heterochromatin-associated nuclear factor in HEV endothelial cells in vivo. Association of IL-33 with heterochromatin was also observed in human and mouse cells under living conditions. In addition, colocalization of IL-33 with mitotic chromatin was noted. Nuclear localization, heterochromatin-association, and targeting to mitotic chromosomes were all found to be mediated by an evolutionarily conserved homeodomain-like helix-turn-helix motif within the IL-33 N-terminal part. Finally, IL-33 was found to possess transcriptional repressor properties, associated with the homeodomain-like helix-turn-helix motif. Together, these data suggest that, similarly to IL1␣ and HMGB1, IL-33 is a dual function protein that may function as both a proinflammatory cytokine and an intracellular nuclear factor with transcriptional regulatory properties.heterochromatin ͉ nucleus ͉ endothelium ͉ HMGB1 C ytokines of the IL-1 family play a major role in a wide range of inflammatory, infectious, and autoimmune diseases (1). The three best known members of this family, IL-1␣, IL-1␤, and IL-18, are highly inflammatory cytokines, and dysregulation of their production or activity can lead to severe pathological events (1, 2). IL-33 is the most recent addition to the IL-1 family (3). IL-33 has been shown to induce T helper (Th) type 2 responses (3) by signaling through the IL-1 receptor-related protein ST2 (IL-1 R4), an orphan member of the IL-1 receptor family (4, 5). Treatment of mice with recombinant IL-33 resulted in blood eosinophilia, splenomegaly, and increased serum levels of IgE, IgA, IL-5, and IL-13 (3). Exposure to IL-33 also caused severe pathological changes in the lungs and gastrointestinal tract, including eosinophilic and mononuclear infiltrates, increased mucus production, and epithelial cell hyperplasia and hypertrophy (3).IL-33 shares with the other members of the IL-1 family a single structural domain formed from 12 ␤ strands, arranged in a so-called IL-1/FGF ␤-trefoil fold (6, 7). Simila...

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“…Accordingly, IL8 binds syndecan-3 (Patterson et al 2005) and syndecan-2 (Halden et al 2004) on the EC surface.…”

Section: Hspgsmentioning

confidence: 98%

Extracellular Angiogenic Growth Factor Interactions: An Angiogenesis Interactome Survey

Rusnati

Presta

2006

Endothelium

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Angiogenesis plays a key role in various physiological and pathological processes, including inflammation and tumor growth. Numerous angiogenic growth factors (AGFs) have been identified. Usually, the angiogenic process is assumed to represent the outcome of a straightforward interaction of AGFs with specific signalling receptors of the endothelial cell (EC) surface. Actually, the mechanisms by which AGFs induce neovascularization are much more complex. Indeed, angiogenesis is the result of the simultaneous actions of various AGFs and angiogenesis modulators; multiple EC surface receptors with different structure and biological properties are engaged by AGFs to exert a full angiogenic response; AGFs bind a variety of free and immobilized proteins, polysaccharides, and complex lipids of the extracellular milieu that affect AGF integrity, stability, and bioavailability; some of the AGF-binding molecules interact also with AGF receptors. In this review the authors summarize literature data and discuss the current knowledge about the extracellular molecules able to interact with AGFs, thus representing possible key regulators of the angiogenesis process and targets/templates for the development of novel antiangiogenic drugs. This work represents an attempt to highlight common theme in the AGF interactome that occurs at the extracellular level during neovascularization.

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Induction of a CXCL8 binding site on endothelial syndecan‐3 in rheumatoid synovium

Cited by 42 publications

References 73 publications

Differential expression of syndecans and glypicans in chronically inflamed synovium

Differential expression of syndecans and glypicans in chronically inflamed synovium

IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factorin vivo

Extracellular Angiogenic Growth Factor Interactions: An Angiogenesis Interactome Survey

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