Expression profles of human CCN genes in patients with osteoarthritis or rheumatoid arthritis

Komatsu, Masatoshi; Nakamura, Yukio; Maruyama, Masaaki; Abe, Kazutoshi; Watanapokasin, Ramida; Kato, Hiroyuki

doi:10.1007/s00776-015-0727-3

Cited by 26 publications

(36 citation statements)

References 36 publications

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“…Platelet activation markers and soluble adhesion molecules are also observed in patients with systemic lupus erythematosus (SLE) (59). Increased recruitment of human CD16 + monocytes into synovial tissues and glomeruli is also seen in rheumatoid arthritis and lupus patients, respectively (6,(60)(61)(62)(63), and murine Ly6C low /Gr1 low monocytes are expanded in the Yaa model of SLE (14). Interestingly, increased soluble CCN1 levels are observed in synovial fluid from rheumatoid arthritis patients (15) and in the serum of SLE patients (64).…”

Section: Discussionmentioning

confidence: 95%

CCN1/CYR61-mediated meticulous patrolling by Ly6C ^low monocytes fuels vascular inflammation

Imhof

Jemelin

Ballet

et al. 2016

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

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Inflammation is characterized by the recruitment of leukocytes from the bloodstream. The rapid arrival of neutrophils is followed by a wave of inflammatory lymphocyte antigen 6 complex (Ly6C)-positive monocytes. In contrast Ly6C low monocytes survey the endothelium in the steady state, but their role in inflammation is still unclear. Here, using confocal intravital microscopy, we show that upon Toll-like receptor 7/8 (TLR7/8)-mediated inflammation of mesenteric veins, platelet activation drives the rapid mobilization of Ly6C low monocytes to the luminal side of the endothelium. After repeatedly interacting with platelets, Ly6C low monocytes commit to a meticulous patrolling of the endothelial wall and orchestrate the subsequent arrival and extravasation of neutrophils through the production of proinflammatory cytokines and chemokines. At a molecular level, we show that cysteine-rich protein 61 (CYR61)/CYR61 connective tissue growth factor nephroblastoma overexpressed 1 (CCN1) protein is released by activated platelets and enables the recruitment of Ly6C low monocytes upon vascular inflammation. In addition endothelium-bound CCN1 sustains the adequate patrolling of Ly6C low monocytes both in the steady state and under inflammatory conditions. Blocking CCN1 or platelets with specific antibodies impaired the early arrival of Ly6C low monocytes and abolished the recruitment of neutrophils. These results refine the leukocyte recruitment cascade model by introducing endothelium-bound CCN1 as an inflammation mediator and by demonstrating a role for platelets and patrolling Ly6C low monocytes in acute vascular inflammation.

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Section: Discussionmentioning

confidence: 95%

CCN1/CYR61-mediated meticulous patrolling by Ly6C ^low monocytes fuels vascular inflammation

Imhof

Jemelin

Ballet

et al. 2016

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

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“…FGF2 adaptor proteins like CCN2, also known as connective tissue growth factor (CTGF), may fine tune FGF2 signaling in mammalian AC [41]. CCN2 mRNA and protein overexpression has been shown in human OA AC compared to healthy AC [50,51]. …”

Section: Fibroblast Growth Factor 2 Signalingmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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Osteoarthritis (OA) is a degenerative whole joint disease, for which no preventative or therapeutic biological interventions are available. This is likely due to the fact that OA pathogenesis includes several signaling pathways, whose interactions remain unclear, especially at disease onset. Early OA is characterized by three key events: a rarely considered early phase of proliferation of cartilage-resident cells, in contrast to well-established increased synthesis, and degradation of extracellular matrix components and inflammation, associated with OA progression. We focused on the question, which of these key events are regulated by growth factors, inflammatory cytokines, and/or miRNA abundance. Collectively, we elucidated a specific sequence of the OA key events that are described best as a very early phase of proliferation of human articular cartilage (AC) cells and concomitant anabolic/catabolic effects that are accompanied by incipient pro-inflammatory effects. Many of the reviewed factors appeared able to induce one or two key events. Only one factor, fibroblast growth factor 2 (FGF2), is capable of concomitantly inducing all key events. Moreover, AC cell proliferation cannot be induced and, in fact, is suppressed by inflammatory signaling, suggesting that inflammatory signaling cannot be the sole inductor of all early OA key events, especially at disease onset.

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“…A growing body of evidence has indicated the involvement of several CCN genes in the pathophysiology of osteoarthritis and RA . Nozawa et al (2009) have found that the serum concentrations of CCN2 were higher in RA .…”

Section: Discussionmentioning

confidence: 99%

Clinical significance of CCN2/connective tissue growth factor in Behçet's disease patients

et al. 2019

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Aim Behçet's disease (BD) is a chronic autoimmune vasculitic disorder of unclear pathogenesis. CCN2/CTGF (connective tissue growth factor) is one of the CCN family members which carry out pro‐angiogenic biological functions and play an important role in inflammatory and autoimmune diseases. The aim of the present study was to assess CCN2 plasma concentrations in BD patients and to analyze their association with clinical features of the disease, activity and laboratory parameters. Methods We included 87 BD patients and 60 healthy control subjects matched for age and gender. Demographic, clinical, disease activity and severity data were recorded. Plasma CCN2 concentrations were measured using enzyme‐linked immunosorbent assay. Results The plasma concentrations of CCN2 in BD patients were significantly elevated compared to healthy controls. The mean plasma CCN2 levels in patients with major organ involvement were significantly higher than those without. Patients who received steroids or cyclophosphamide showed a significant reduction in CCN2 levels. This was confirmed by the results of multivariate analysis. Patients with active ocular disease had a significant increase in CCN2 compared to the inactive group. On the other hand, CCN2 levels were not significantly correlated with overall disease activity and severity scores. Conclusion Behçet's disease patients showed a significant increase of CCN2 levels, especially in the group of patients with major organ involvement. A significant reduction of these levels was found in patients who received steroids or cyclophosphamide. Larger studies with further investigations of the precise role of CCN2 in BD pathogenesis might lead to novel therapies for the clinical management of this disease.

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Expression profles of human CCN genes in patients with osteoarthritis or rheumatoid arthritis

Cited by 26 publications

References 36 publications

CCN1/CYR61-mediated meticulous patrolling by Ly6C ^low monocytes fuels vascular inflammation

CCN1/CYR61-mediated meticulous patrolling by Ly6C ^low monocytes fuels vascular inflammation

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Clinical significance of CCN2/connective tissue growth factor in Behçet's disease patients

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Expression profles of human CCN genes in patients with osteoarthritis or rheumatoid arthritis

Cited by 26 publications

References 36 publications

CCN1/CYR61-mediated meticulous patrolling by Ly6C low monocytes fuels vascular inflammation

CCN1/CYR61-mediated meticulous patrolling by Ly6C low monocytes fuels vascular inflammation

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Clinical significance of CCN2/connective tissue growth factor in Behçet's disease patients

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CCN1/CYR61-mediated meticulous patrolling by Ly6C ^low monocytes fuels vascular inflammation

CCN1/CYR61-mediated meticulous patrolling by Ly6C ^low monocytes fuels vascular inflammation