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2.5 kDa and 5.0 kDa heparin fragments specifically inhibit microvessel sprouting and network formation in VEGF~165~‐mediated mammalian angiogenesis by Klas Norrby is a scholarly article available to read on EtoBox.

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Tumour growth is angiogenesis dependent. Thrombosis and thromboembolism are very common in cancer patients. These patients are often treated with heparin as an anti‐coagulant. Many tumour angiogens, including VEGF~165~, and endogenous anti‐angiogenesis factors bind heparin tightly. Using the non‐surgical mesenteric‐window angiogenesis assay, we studied in detail the systemic effect of heparin fractions with a mean MW of 2.5, 5.0 and 16.4 kDa on the microvessel sprouting and network formation in angiogenesis mediated by VEGF~165~ in rats. The microvessel network was assessed objectively in terms of the number and lengths of segments (the distance between two successive branching points), the number of branching points, the degree of tortuosity, the index of interconnecting loop formation, the index of intersection, as well as the number and lengths of sprouts. Compared with the saline control, the 2.5 kDa fraction significantly shortened the microvessel sprouts and the microvessel segments but increased the microvessel tortuosity in statistical terms; the 5.0 kDa fraction statistically significantly shortened the sprouts, decreased the number of segments and the number of microvesse

Author

Klas Norrby

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0959-9673)

Published

2000

Language

EN