Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions (Articolo in rivista)

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  • Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions (Articolo in rivista) (literal)
Anno
  • 2001-01-01T00:00:00+01:00 (literal)
Alternative label
  • Carmeliet et al. (2001)
    Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions
    in Nature medicine (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Carmeliet et al. (literal)
Pagina inizio
  • 575 (literal)
Pagina fine
  • 583 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 7 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto
  • Identificazione del ruolo di Plgf nelcontrollo dell'angogenesi patologica in diverse condizioni quali ischemia, tumori, retinopatie. (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Carmeliet P1, Moons L1, Luttun A1, Vincenti V2, Compernolle V1, De Mol M1, Wu Y3, Bono F4, Devy L5, Beck H6, Scholz D7, Acker T6, DiPalma T2, Dewerchin M1, Noel A5, Stalmans I1, Barra A2, Blacher S5, Vandendriessche T1, Ponten A9, Eriksson U9, Plate KH6, Foidart JM5, Schaper W7, Charnock-Jones DS8, Hicklin DJ3, Herbert JM4, Collen D1, Persico MG2 1 VIB; 2CNR; 3 ImClone Systems; 4 Sanofi; 5. University Liège; 6. FAU Erlangen-Nürnberg; 7 Max-Planck-Institute; 8 University Cambridge, 9 LICR (literal)
Titolo
  • Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions (literal)
Abstract
  • Vascular endothelial growth factor (VEGF) stimulates angiogenesis by activating VEGF receptor-2 (VEGFR-2). The role of its homolog, placental growth factor (PlGF), remains unknown. Both VEGF and PlGF bind to VEGF receptor-1 (VEGFR-1), but it is unknown whether VEGFR-1, which exists as a soluble or a membrane-bound type, is an inert decoy or a signaling receptor for PlGF during angiogenesis. Here, we report that embryonic angiogenesis in mice was not affected by deficiency of PlGF (Pgf-/-). VEGF-B, another ligand of VEGFR-1, did not rescue development in Pgf-/- mice. However, loss of PlGF impaired angiogenesis, plasma extravasation and collateral growth during ischemia, inflammation, wound healing and cancer. Transplantation of wild-type bone marrow rescued the impaired angiogenesis and collateral growth in Pgf-/- mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow-derived cells. The synergism between PlGF and VEGF was specific, as PlGF deficiency impaired the response to VEGF, but not to bFGF or histamine. VEGFR-1 was activated by PlGF, given that anti-VEGFR-1 antibodies and a Src-kinase inhibitor blocked the endothelial response to PlGF or VEGF/PlGF. By upregulating PlGF and the signaling subtype of VEGFR-1, endothelial cells amplify their responsiveness to VEGF during the 'angiogenic switch' in many pathological disorders. (literal)
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