| First Author | Zimrin AB | Year | 1996 |
| Journal | J Biol Chem | Volume | 271 |
| Issue | 51 | Pages | 32499-502 |
| PubMed ID | 8955070 | Mgi Jnum | J:113824 |
| Mgi Id | MGI:3687705 | Doi | 10.1074/jbc.271.51.32499 |
| Citation | Zimrin AB, et al. (1996) An antisense oligonucleotide to the notch ligand jagged enhances fibroblast growth factor-induced angiogenesis in vitro. J Biol Chem 271(51):32499-502 |
| abstractText | Angiogenesis, or the formation of new blood vessels, plays a central role in a number of physiologic and pathologic conditions, including wound healing, diabetic retinopathy, and solid tumor growth, and endothelial cells can be induced to mimic this process in vitro. Using a modification of the differential display method (Zimrin, A. B., Villeponteau, B., and Maciag, T. (1995) Biochem. Biophys. Res. Commun. 213, 630-638), we isolated the human homolog of the Jagged ligand for the Notch receptor from human endothelial cells exposed to fibrin and demonstrate that the Jagged transcript, but not the Notch 1 or Notch 2 transcripts, are up-regulated by fibrin. Interestingly, the addition of an antisense Jagged oligomer to bovine microvascular endothelial cells grown on a collagen gel resulted in a marked increase in invasion and tube formation in the underlying gel in response to fibroblast growth factor. In contrast, no effect was observed on vascular endothelial growth factor-induced angiogenesis under identical conditions. These data suggest that Jagged-Notch signaling is able to regulate fibroblast growth factor-induced endothelial cell migration in vitro, an early event during angiogenesis in vivo. |
