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  • Carmeliet, Peter (author)

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

  • Article/chapterEnglish2001

Publisher, publication year, extent ...

  • 2001-05-01
  • Springer Science and Business Media LLC,2001

Numbers

  • LIBRIS-ID:oai:lup.lub.lu.se:18665b1e-53c1-4d52-9c09-51299501c7f3
  • https://lup.lub.lu.se/record/1121192URI
  • https://doi.org/10.1038/87904DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:17600041URI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • 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.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Moons, Lieve (author)
  • Luttun, Aernout (author)
  • Vincenti, Valeria (author)
  • Compernolle, Veerle (author)
  • De Mol, Maria (author)
  • Wu, Yan (author)
  • Bono, Françoise (author)
  • Devy, Laetitia (author)
  • Beck, Heike (author)
  • Scholz, Dimitri (author)
  • Acker, Till (author)
  • DiPalma, Tina (author)
  • Dewerchin, Mieke (author)
  • Noel, Agnes (author)
  • Stalmans, Ingeborg (author)
  • Barra, Adriano (author)
  • Blacher, Sylvia (author)
  • Vandendriessche, Thierry (author)
  • Pontén, AnnicaLund University,Lunds universitet,Stamcellscentrum (SCC),Avdelningen för stamcellsforskning,Institutionen för laboratoriemedicin,Medicinska fakulteten,Stem Cell Center,Division of stem cell research,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)med-anp (author)
  • Eriksson, UlfKarolinska Institutet (author)
  • Plate, Karl H. (author)
  • Foidart, Jean-Michel (author)
  • Schaper, Wolfgang (author)
  • Charnock-Jones, D. Stephen (author)
  • Hicklin, Daniel J. (author)
  • Herbert, Jean-Marc (author)
  • Collen, Désiré (author)
  • Persico, M. Graziella (author)
  • Stamcellscentrum (SCC)Avdelningen för stamcellsforskning (creator_code:org_t)

Related titles

  • In:Nature Medicine: Springer Science and Business Media LLC7:5, s. 575-5831546-170X1078-8956

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