Abstract
The exact mechanisms of the angiostatic effect by tecogalan sodium (TS) remain unclear. We examined the effects of TS on in vitro angiogenic activity, proteolytic activity and proliferation of retinal vascular endothelial cells (RECs). TS markedly inhibited the in vitro angiogenic activity of RECs although the growth inhibition of RECs was small. TS apparently decreased the cell-associated urokinase-type plasminogen activator (uPA) activity and matrix metalloprotease 1 (MMP-1) activity even in the presence of anti-bFGF IgG. Thus, the suppression of the periendothelial matrix-degrading activities related to uPA and MMP-1 is suggested to be another possible mechanism of the antiangiogenic effect of TS, besides its prevention of bFGF REC binding which has previously been reported.
Copyright 2000 S. Karger AG, Basel
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology*
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Blotting, Northern
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Cattle
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Cell Division / drug effects
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Cells, Cultured
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Endothelium, Vascular / drug effects*
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Endothelium, Vascular / enzymology
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Gelatinases / metabolism
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Matrix Metalloproteinase 1 / genetics
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Matrix Metalloproteinase 1 / metabolism
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Neovascularization, Pathologic / pathology
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Neovascularization, Pathologic / prevention & control*
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Peptide Hydrolases / metabolism*
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Polysaccharides, Bacterial / pharmacology*
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RNA, Messenger / metabolism
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Retinal Vessels / cytology
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Retinal Vessels / drug effects*
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Thymidine / metabolism
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Urokinase-Type Plasminogen Activator / metabolism
Substances
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Antineoplastic Agents
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Polysaccharides, Bacterial
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RNA, Messenger
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tecogalan
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Peptide Hydrolases
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Urokinase-Type Plasminogen Activator
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Gelatinases
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Matrix Metalloproteinase 1
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Thymidine