| First Author | Kiba A | Year | 2003 |
| Journal | Biochem Biophys Res Commun | Volume | 301 |
| Issue | 2 | Pages | 371-7 |
| PubMed ID | 12565870 | Mgi Jnum | J:82135 |
| Mgi Id | MGI:2451210 | Doi | 10.1016/s0006-291x(02)03033-4 |
| Citation | Kiba A, et al. (2003) VEGFR-2-specific ligand VEGF-E induces non-edematous hyper-vascularization in mice. Biochem Biophys Res Commun 301(2):371-7 |
| abstractText | VEGF family members play important roles in angiogenesis and vascular permeability. VEGF-A-transgenic mice showed an increased vascularization with edema due to hyper-vascular permeability and subcutaneous hemorrhage as side effects. VEGF-A binds and activates two receptors, VEGFR-1 (Flt-1) and VEGFR-2 (KDR/Flk-1). To dissect the signals of these two receptors, we generated transgenic mice overexpressing either the VEGFR-2-specific ligand VEGF-E(NZ-7) or VEGFR-1-specific ligand PlGF-II under the control of the Keratin-14 promoter. VEGF-E-mice showed a significant increase in vascularization (about 10-fold compared to control mice) in subcutaneous tissues, whereas PlGF-mice showed only a 2-3-fold increase. Interestingly, VEGF-E-mice did not show any clear edematous lesions or hemorrhagic spots on the skin. Microscopically, VEGF-E-induced capillary networks have a well organized structure with the recruitment of pericytes. These results indicate that VEGF-E is a new angiogenic agent with less side effects for clinical usage. |
