Neutralization of Vascular Endothelial Growth Factor Prevents Collagen-Induced Arthritis and Ameliorates Established Disease in Mice

Sone, Hirohito; Kawakami, Yasushi; Sakauchi, Michihiro; Nakamura, Yasushi; Takahashi, Akimitsu; Shimano, Hitoshi; Okuda, Yukichi; Segawa, Toshiaki; Suzuki, Hideo; Yamada, Nobuhiro

doi:10.1006/bbrc.2001.4395

Cited by 104 publications

(75 citation statements)

References 17 publications

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“…The synovial events affected by the presence of the Cia5a or Cia5d intervals have been previously shown to be at least in part interdependent. Specifically, angiogenesis is a critical event in the pathogenesis of autoimmune arthritis and in the development of synovial hyperplasia (47,48). Similarly, synovial hyperplasia and pannus formation are typically associated with cartilage and bone erosions in arthritis (41,49), and are partially dependent on the inflammatory mononuclear cellular infiltrate and the cytokines these infiltrating cells produce (50 -53).…”

Section: Discussionmentioning

confidence: 99%

The Non-MHC Quantitative Trait LocusCia5Contains Three Major Arthritis Genes That Differentially Regulate Disease Severity, Pannus Formation, and Joint Damage in Collagen- and Pristane-Induced Arthritis

Meng

Yarlett

Joe

et al. 2005

The Journal of Immunology

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Cia5 is a locus on rat chromosome 10 which regulates the severity of collagen- and pristane-induced arthritis (CIA and PIA). To refine the region toward positional identification, Cia5 subcongenic strains were generated and studied in PIA and CIA. The protective effect of the telomeric locus Cia5a was confirmed in both models. A second arthritis severity locus (Cia5d) was identified within the most centromeric portion of Cia5. DA.F344(Cia5d) rats had a significantly lower median arthritis severity index in PIA, but not in CIA, compared with DA. On histologic analyses DA.F344(Cia5a) and DA.F344(Cia5d) congenics with PIA preserved a nearly normal joint architecture compared with DA, including significant reduction in synovial hyperplasia, pannus, angiogenesis, inflammatory infiltration, bone and cartilage erosions. Cia5 and Cia5a synovial levels of IL-1β mRNA were reduced. Although both DA.F344(Cia5) and DA.F344(Cia5a) rats were protected in CIA, the arthritis scores of DA.F344(Cia5) were significantly higher than those of DA.F344(Cia5a), suggesting the existence of a third locus where F344-derived alleles centromeric from Cia5a contribute to increased arthritis severity. The existence of the third locus was further supported by higher levels of autoantibodies against rat type II collagen in DA.F344(Cia5) congenics compared with DA.F344(Cia5a). Our results determined that Cia5 contains three major arthritis severity regulatory loci regulating central events in the pathogenesis of arthritis, and differentially influencing CIA and PIA. These loci are syntenic to regions on human chromosomes 17q and 5q implicated in the susceptibility to rheumatoid arthritis, suggesting that the identification of these genes will be relevant to human disease.

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Section: Discussionmentioning

confidence: 99%

The Non-MHC Quantitative Trait LocusCia5Contains Three Major Arthritis Genes That Differentially Regulate Disease Severity, Pannus Formation, and Joint Damage in Collagen- and Pristane-Induced Arthritis

Meng

Yarlett

Joe

et al. 2005

The Journal of Immunology

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“…29 Direct blockade of VEGF in CIA has also been achieved using polyclonal anti-VEGF antibodies raised in rabbits. 30,31 Finally, K1-5 (protease-activated kringles 1-5), an angiogenesis inhibitor related to angiostatin directly acting on endothelium, significantly reduced both the paw swelling and the clinical score in CIA. The efficacy of this treatment was reflected in a reduction in joint inflammation and destruction, as assessed histologically.…”

Section: Discussionmentioning

confidence: 99%

Adenoviral delivery of soluble VEGF receptor 1 (sFlt-1) abrogates disease activity in murine collagen-induced arthritis

2003

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“…This treatment paradigm is supported by numerous animal studies demonstrating that antiangiogenic agents significantly suppress both the incidence and the severity of disease (23)(24)(25)(26)(27)(28)(29). The most efficient means of adding angiogenesis inhibitors to the clinical armamentarium for RA would be to determine whether current therapies exhibit anti-angiogenic properties.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous animal studies indicate that antiangiogenic treatments effectively reduce both the incidence and the severity of collagen-induced arthritis (CIA) (23)(24)(25)(26)(27) and adjuvant-induced arthritis (AIA) (28,29). The present study compared the antiangiogenic activities of anti-IL-1 and anti-TNF␣ biologic agents in conventional models of arthritis and vascular growth factor-induced neovascularization.…”

mentioning

confidence: 96%

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

Coxon¹,

Bolon²,

Estrada³

et al. 2002

Arthritis & Rheumatism

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Objective. To assess the capacities of the cytokine inhibitors interleukin-1 receptor antagonist (IL-1Ra; anakinra) and PEGylated soluble tumor necrosis factor receptor I (PEG sTNFRI; pegsunercept) to suppress neovascularization.Methods. A corneal angiogenesis assay was performed by implanting nylon discs impregnated with an angiogenic stimulator (basic fibroblast growth factor or vascular endothelial growth factor) into one cornea of female Sprague-Dawley rats. Animals were treated with IL-1Ra or PEG sTNFRI for 7 days, after which new vessels were quantified. In a parallel study, male Lewis rats with mycobacteria-induced adjuvant-induced arthritis were treated with IL-1Ra or PEG sTNFRI for 7 days beginning at disease onset, after which scores for inflammation and bone erosion as well as capillary counts were acquired from sections of arthritic hind paws.Results. Treatment with IL-1Ra yielded a dosedependent reduction in growth factor-induced corneal angiogenesis, while PEG sTNFRI did not. IL-1Ra, but not PEG sTNFRI, significantly reduced the number of capillaries in arthritic paws, even though both anticytokines reduced inflammation and bone erosion to a similar degree.Conclusion. These data support a major role for IL-1, but not TNF␣, in angiogenesis and suggest that an additional antiarthritic mechanism afforded by IL-1 inhibitors, but not anti-TNF agents, is the suppression of the angiogenic component of pannus.

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Neutralization of Vascular Endothelial Growth Factor Prevents Collagen-Induced Arthritis and Ameliorates Established Disease in Mice

Cited by 104 publications

References 17 publications

The Non-MHC Quantitative Trait LocusCia5Contains Three Major Arthritis Genes That Differentially Regulate Disease Severity, Pannus Formation, and Joint Damage in Collagen- and Pristane-Induced Arthritis

The Non-MHC Quantitative Trait LocusCia5Contains Three Major Arthritis Genes That Differentially Regulate Disease Severity, Pannus Formation, and Joint Damage in Collagen- and Pristane-Induced Arthritis

Adenoviral delivery of soluble VEGF receptor 1 (sFlt-1) abrogates disease activity in murine collagen-induced arthritis

Inhibition of interleukin‐1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis

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