The role of plasminogen in angiogenesis in vivo

• Published in: Journal of thrombosis and haemostasis 2003-08, Vol.1 (8), p.1683-1687
• Main Authors: Oh, C.‐W, Hoover‐Plow, J, Plow, E. F
• Format: Article
• Language: English
• Subjects: Animals; Cornea - metabolism; Extracellular Matrix - metabolism; Female; Fibroblast Growth Factor 2 - metabolism; Genotype; Humans; in vivo angiogenesis; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; mouse corneal model; Neovascularization, Physiologic; Plasminogen - metabolism; Plasminogen - physiology; plasminogen deficient mice; Receptors, Cell Surface - metabolism; Receptors, Urokinase Plasminogen Activator; Time Factors; urokinase; urokinase receptor; Urokinase-Type Plasminogen Activator - metabolism
• ISSN: 1538-7933; 1538-7836; 1538-7836
• DOI: 10.1046/j.1538-7836.2003.00182.x

Plasminogen, by virtue of its role in the degradation of extracellular matrix proteins and by facilitation of cell migration, may contribute to angiogenesis. Objective: the purpose of this study was to evaluate the contribution of plasminogen to angiogenesis in vivo. Methods: Angiogenesis was assessed in gene‐targeted mice with deficiencies of plasminogen, urokinase plasminogen activator (uPA), and urokinase receptor (uPAR) in a mouse corneal model. In wild‐type mice, female and young mice showed a trend toward increased angiogenesis compared to males and old mice. Because of this influence of age and gender on angiogenesis, young, female mice (6–13 weeks of age) were used for this study. Results: In response to angiogenic stimulation by basic fibroblast growth factor (bFGF), uPA deficient mice exhibited a decrease in new vessel formation as reflected by vessel length (0.47 in control vs. 0.33 mm in uPA−/− mice, P = 0.043), but new vessel formation was not altered (P = 0.107) in the uPAR deficient mice compared to control mice. A significantly decreased angiogenic response of new vessel formation to both vascular endothelial growth factor (VEGF) (P