| First Author | Oh CW | Year | 2003 |
| Journal | J Thromb Haemost | Volume | 1 |
| Issue | 8 | Pages | 1683-7 |
| PubMed ID | 12911578 | Mgi Jnum | J:128184 |
| Mgi Id | MGI:3766371 | Doi | 10.1046/j.1538-7836.2003.00182.x |
| Citation | Oh CW, et al. (2003) The role of plasminogen in angiogenesis in vivo. J Thromb Haemost 1(8):1683-7 |
| abstractText | 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 < 0.02) and bFGF (P < 0.007) was observed in Plg deficient (Plg-/-) mice (VEGF - 0.36 mm, bFGF - 0.67 mm) compared to Plg+/+ mice (VEGF - 0.56 mm, bFGF - 0.85 mm). CONCLUSIONS: These results demonstrate the importance of plasminogen, as well as of uPA, in angiogenesis in vivo. |
