Angiogenesis stimulated by PDGF-CC, a novel member in the PDGF family, involves activation of PDGFR-alphaalpha and -alphabeta receptors.
FASEB J
; 16(12): 1575-83, 2002 Oct.
Article
em En
| MEDLINE
| ID: mdl-12374780
ABSTRACT
A newly discovered PDGF isoform, PDGF-CC, is expressed in actively angiogenic tissues such as placenta, some embryonic tissues, and tumors. We test the possibility that PDGF-CC promotes angiogenesis in vivo. The core domain (mature form) of human PDGF-CC is sufficiently potent to stimulate neovascularization in the mouse cornea. The corneal angiogenic response induced by PDGF-CC is robust although the area of neovascularization is smaller than those of FGF-2- and VEGF-stimulated angiogenesis. Similarly, PDGF-BB and PDGF-AB induce angiogenic responses virtually indistinguishable from PDGF-CC-stimulated vessels. In contrast, PDGF-AA displays only a weak angiogenic response in the mouse cornea. Although there was no significant difference in incorporation of mural cells to the newly formed blood vessels induced by PDGF-BB and -CC, the percentage of mural cell positive vessels induced by PDGF-AA was greater than those induced by FGF-2, PDGF-BB, and PDGF-CC. In the developing chick embryo, PDGF-CC induced branch sprouts from established blood vessels. In PDGF receptor-transfected endothelial cells, PDGF-CC activated the PDGF receptor alpha subunit (PDGFR-alpha). PDGF-CC, but not PDGF-AA, was able to activate PDGFR-beta receptor in endothelial cells that coexpress both alpha and beta forms of receptors. Thus, the PDGF-CC-mediated angiogenic response is most likely transduced by PDGF-alphaalpha and -alphabeta receptors. These data demonstrate that the PDGF family is a complex and important group of proangiogenic factors.
Buscar no Google
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fator de Crescimento Derivado de Plaquetas
/
Receptor alfa de Fator de Crescimento Derivado de Plaquetas
/
Neovascularização Patológica
Idioma:
En
Revista:
FASEB J
Ano de publicação:
2002
Tipo de documento:
Article