Kinetics of circulating endothelial progenitor cells in mice with type II collagen arthritis

Kurosaka, Daitaro; Yasuda, Jun; Yoshida, Ken; Yasuda, Chiho; Toyokawa, Yasuhiko; Yokoyama, T.; Kingetsu, Isamu; Yamada, Akio

doi:10.1016/j.bcmd.2005.06.001

Cited by 8 publications

(7 citation statements)

References 15 publications

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“…In an earlier study that used a similar CIA model, EPCs were also elevated in the peripheral blood of mice at the time of disease onset (20). However, in that study, EPCs were not elevated prior to the onset of clinically identifiable symptoms or 1 week after arthritis was established, when disease severity scores were maximal.…”

Section: Discussionmentioning

confidence: 69%

“…In contrast, we found that EPCs were significantly elevated 2-21 days post-inflammation onset in animals with arthritis. This difference could be due to the use of slightly different CIA induction protocols, or could reflect the fact that CD117 was used as the EPC-defining marker in the earlier study (20), whereas we used Sca-1 for EPC identification in peripheral blood. Nonetheless, taken together these data suggest that EPCs are mobilized into the circulation during arthritis pathogenesis, are recruited to the inflamed synovium, and may contribute to disease progression.…”

Section: Discussionmentioning

confidence: 99%

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The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

Silverman¹,

Haas²,

Rad³

et al. 2007

Arthritis & Rheumatism

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Objective. Marrow-derived endothelial progenitor cells (EPCs) are important in the neovascularization that occurs in diverse conditions such as cardiovascular disorders, inflammatory diseases, and neoplasms. In rheumatoid arthritis (RA), synovial neovascularization propels disease by nourishing the inflamed and hyperproliferative synovium. This study was undertaken to investigate the hypothesis that EPCs selectively home to inflamed joint tissue and may perpetuate synovial neovascularization.Methods. In a collagen-induced arthritis (CIA) model, neovascularization and EPC accumulation in mouse ankle synovium was measured. In an antibodyinduced arthritis model, EPC recruitment to inflamed synovium was evaluated. In a chimeric SCID mouse/ human synovial tissue (ST) model, mice were engrafted subcutaneously with human ST, and EPC homing to grafts was assessed 2 days later. EPC adhesion to RA fibroblasts and RA ST was evaluated in vitro.Results. In mice with CIA, cells bearing EPC markers were significantly increased in peripheral blood and accumulated in inflamed synovial pannus. EPCs were 4-fold more numerous in inflamed synovium from mice with anti-type II collagen antibody-induced arthritis versus controls. In SCID mice, EPC homing to RA ST was 3-fold greater than to normal synovium. Antibody neutralization of vascular cell adhesion molecule 1 (VCAM-1) and its ligand component ␣4 integrin potently inhibited EPC adhesion to RA fibroblasts and RA ST cryosections.Conclusion. These data demonstrate the selective recruitment of EPCs to inflamed joint tissue. The VCAM-1/very late activation antigen 4 adhesive system critically mediates EPC adhesion to cultured RA fibroblasts and to RA ST cryosections. These findings provide evidence of a possible role of EPCs in the synovial neovascularization that is critical to RA pathogenesis.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

Silverman¹,

Haas²,

Rad³

et al. 2007

Arthritis & Rheumatism

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“…For example, angiostatin gene transfer attenuated murine CIA [6,108]. Endostatin both prophylactically and therapeutically suppressed arthritis scores, pannus formation and the development of joint erosions in rodent arthritis models [6,107,109,111,112]. The angiostatin-like protease-activated kringles 1-5 (K1-5) may be a more potent angiogenesis inhibitor than angiostatin itself [113].…”

Section: Angiogenesis Inhibitors and Their Use In Arthritis Therapymentioning

confidence: 99%

Angiogenesis in rheumatoid arthritis

et al. 2009

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Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, matrix components, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiogenic chemokines, tumor necrosis factor-α and the α V β 3 integrin may attenuate the action of angiogenic mediators and thus synovial angiogenesis. In addition, some naturally produced or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide may be included in the management of RA.

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“…13,85 The presence of EPCs in the synovial tissue of patients with RA or osteoarthritis provides further evidence that vasculogenesis might be induced by precursor cells that arise in situ or from circu lating progenitors. 12 The preferential homing of EPCs to inflamed synovium was found to be mediated at least in part by the interaction between vascular cell adhesion molecule-1 and α 4 -integrin on activated fibroblasts and EPCs.…”

Section: Epc Homing To Arthritic Jointsmentioning

confidence: 98%

Endothelial progenitor cell dysfunction in rheumatic disease

Westerweel

Verhaar

2009

Nat Rev Rheumatol

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Rheumatic disease is characterized by inflammation and endothelial dysfunction, which contribute to accelerated atherosclerosis. Circulating endothelial progenitor cells (EPCs) can restore dysfunctional endothelium and thereby protect against atherosclerotic vascular disease. The number and function of EPCs are, however, affected in rheumatic diseases such as psoriatic arthritis, rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, and antineutrophil cytoplasmic autoantibody-associated vasculitis. rheumatic disease is often characterized by decreased numbers, and impaired function, of EPCs, although numbers of these cells might increase during the initial years of systemic sclerosis. Pioneering studies show that EPC dysfunction might be improved with pharmacological treatment. How best to restore EPC function, and whether achieving this aim can prevent long-term cardiovascular complications in rheumatic disease, remain to be established.

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Kinetics of circulating endothelial progenitor cells in mice with type II collagen arthritis

Cited by 8 publications

References 15 publications

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

Angiogenesis in rheumatoid arthritis

Endothelial progenitor cell dysfunction in rheumatic disease

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