Inhibition of human endothelial cell proliferation by gold compounds.

Matsubara, Tsukasa; Ziff, Morris

doi:10.1172/jci112972

Cited by 65 publications

(24 citation statements)

References 39 publications

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“…These include cytokines, such as basic fibroblast growth factor (bFGF) (5), interleukin-8, and vascular endothelial growth factor, and soluble adhesion molecules, such as vascular cell adhesion molecule and Eselectin (6). Interestingly, many of the available treatments for RA have been shown to possess some degree of antiangiogenic activity (7)(8)(9). In fact, treatments that suppress the angiogenic process may favorably impact disease course, as suggested by studies in an adjuvant-induced model of arthritis (10).…”

Section: Introductionmentioning

confidence: 99%

Decreased angiogenesis and arthritic disease in rabbits treated with an αvβ3 antagonist

Storgard¹,

Stupack²,

Jonczyk³

et al. 1999

J. Clin. Invest.

294

198

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Rheumatoid arthritis (RA) is an inflammatory disease associated with intense angiogenesis and vascular expression of integrin αvβ3. Intra-articular administration of a cyclic peptide antagonist of integrin αvβ3 to rabbits with antigen-induced arthritis early in disease resulted in inhibition of synovial angiogenesis and reduced synovial cell infiltrate, pannus formation, and cartilage erosions. These effects were not associated with lymphopenia or impairment of leukocyte function. Furthermore, when administered in chronic, preexisting disease, the αvβ3 antagonist effectively diminished arthritis severity and was associated with a quantitative increase in apoptosis of the angiogenic blood vessels. Therefore, angiogenesis appears to be a central factor in the initiation and persistence of arthritic disease, and antagonists of integrin αvβ3 may represent a novel therapeutic strategy for RA.

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Section: Introductionmentioning

confidence: 99%

Decreased angiogenesis and arthritic disease in rabbits treated with an αvβ3 antagonist

Storgard¹,

Stupack²,

Jonczyk³

et al. 1999

J. Clin. Invest.

294

198

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“…GSTM inhibits monocyte oxygen radical generation (19) and Fc and C3 receptor expression and chemotaxis (20). Moreover, GSTM has effects on endothelial cells including inhibition of cell proliferation (21) and HLA-DR expression (22).…”

Section: Introductionmentioning

confidence: 99%

Effect of gold sodium thiomalate and its thiomalate component on the in vitro expression of endothelial cell adhesion molecules.

Newman¹,

To²,

Robinson³

et al. 1994

J. Clin. Invest.

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Endothelial adhesion molecules play an important role in the tissue recruitment of leukocytes in inflammatory conditions such as rheumatoid arthritis. We have investigated the effect of the antirheumatic drug gold sodium thiomalate on adhesion molecule protein and mRNA expression in cultured human endothelial cells. Gold sodium thiomalate inhibited cytokine (TNF, IL-1, IL-4)-stimulated expression of vascular cell adhesion molecule-i and E-selectin but not intercellular adhesion molecule-i on endothelial cells. Gold sodium thiomalate also suppressed TNF-stimulated increases in vascular cell adhesion molecule-i and E-selectin mRNA levels but had no effect on intercellular adhesion molecule-i mRNA. Thiomalate (mercaptosuccinate), but not gold thioglucose or D-penicillamine, mimics the effect of gold sodium thiomalate at equimolar concentrations. We propose that the inhibition of vascular cell adhesion molecule-i and E-selectin expression by gold sodium thiomalate is due to its thiomalate and not its gold component. Gold sodium thiomalate has a direct effect on endothelial adhesion molecule expression, and this may contribute to its antiinflammatory activity. (J.

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“…These results indicate that EC are more sensitive to CCA than are synovial fibroblasts. We (28) and others (29) have reported that gold sodium thiomalate inhibits the proliferation of EC. It has also been shown that D-penicillamine and methotrexate inhibit both basal and endothelial cell growth factor (ECGF)-stimulated DNA synthesis by human EC in vitro and suppress ECGF-induced neovascularization in vivo (30,3 1).…”

Section: Discussionmentioning

confidence: 75%

Effects of lobenzarit disodium on human endothelial cells. Lobenzarit disodium inhibits proliferative response, HLA–DR antigen expression, and T cell adherence toward endothelial cells

Kawakami

Eguchi

Ueki

et al. 1991

Arthritis & Rheumatism

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The therapeutic action of lobenzarit disodium (CCA) on the function of endothelial cells (EC) isolated from human umbilical cord veins was investigated. CCA suppressed 3H‐thymidine incorporation into EC in a dose‐dependent manner. Significant inhibition was detected at a concentration of 50 μg/ml. The expression of HLA–DR antigen on the surface of EC was increased when EC were cultured with recombinant interferon‐γ (rIFNγ). Treatment of EC with either IFNγ or interleukin‐1 enhanced the adhesion of T cells to EC. The kinetics of HLA–DR antigen expression by EC cultured with IFNγ was different from the kinetics of T cell‐EC adhesion, however. Neither anti–HLA–DR nor anti–HLA–ABC monoclonal antibody inhibited T cell binding to EC monolayers. CCA suppressed the expression of HLA–DR antigen by EC cultured with rIFNγ. In an EC monolayer adhesion assay, CCA also inhibited T cell adhesion to EC in the presence of either IFNγ or interleukin‐1. Significant inhibition was observed at a CCA concentration of 10 μg/ml, a level that is easily attainable in serum. These results suggest that CCA may suppress rheumatoid synovitis by reducing the angiogenesis and emigration of chronic inflammatory cells from the blood into the synovium.

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Inhibition of human endothelial cell proliferation by gold compounds.

Cited by 65 publications

References 39 publications

Decreased angiogenesis and arthritic disease in rabbits treated with an αvβ3 antagonist

Decreased angiogenesis and arthritic disease in rabbits treated with an αvβ3 antagonist

Effect of gold sodium thiomalate and its thiomalate component on the in vitro expression of endothelial cell adhesion molecules.

Effects of lobenzarit disodium on human endothelial cells. Lobenzarit disodium inhibits proliferative response, HLA–DR antigen expression, and T cell adherence toward endothelial cells

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