| pubmed-article:11549592 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11549592 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:11549592 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
| pubmed-article:11549592 | lifeskim:mentions | umls-concept:C0302600 | lld:lifeskim |
| pubmed-article:11549592 | lifeskim:mentions | umls-concept:C1801960 | lld:lifeskim |
| pubmed-article:11549592 | lifeskim:mentions | umls-concept:C0378516 | lld:lifeskim |
| pubmed-article:11549592 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:11549592 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:11549592 | pubmed:dateCreated | 2001-9-10 | lld:pubmed |
| pubmed-article:11549592 | pubmed:abstractText | The known responses of vascular endothelial growth factor (VEGF) are mediated through VEGF receptor-2 (VEGFR-2/KDR) in endothelial cells. However, it is unknown whether VEGFR-1 (Flt-1) is an inert decoy or a signaling receptor for VEGF during physiological or pathological angiogenesis. Here we report that VEGF-stimulated nitric oxide (NO) release is inhibited by blockade of VEGFR-1 and that VEGFR-1 via NO negatively regulates of VEGFR-2-mediated proliferation and promotes formation of capillary networks in human umbilical vein endothelial cells (HUVECs). Inhibition of VEGFR-1 in a murine Matrigel angiogenesis assay induced large aneurysm-like structures. VEGF-induced capillary growth over 14 days was inhibited by anti-VEGFR-2-blocking antibody as determined by reduced tube length between capillary connections (P < 0.0001) in an in vitro angiogenesis assay. In contrast, loss of VEGFR-1 activity with a neutralizing anti-VEGFR-1 antibody resulted in an increase in the accumulation of endothelial cells (P < 0.0001) and a dramatic decrease in the number of capillary connections that were restored by the addition of NO donor. Porcine aortic endothelial (PAE) cells expressing human VEGFR-1 but not VEGFR-2 plated on growth factor-reduced Matrigel rearranged into tube-like structures that were prevented by anti-VEGFR-1 antibody or a cGMP inhibitor. VEGF stimulated NO release from VEGFR-1- but not VEGFR-2-transfected endothelial cells and placenta growth factor-1 stimulated NO release in HUVECs. Blockade of VEGFR-1 increased VEGF-mediated HUVEC proliferation that was inhibited by NO donors, and potentiated by NO synthase inhibitors. These data indicate that VEGFR-1 is a signaling receptor that promotes endothelial cell differentiation into vascular tubes, in part by limiting VEGFR-2-mediated endothelial cell proliferation via NO, which seems to be a molecular switch for endothelial cell differentiation. | lld:pubmed |
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| pubmed-article:11549592 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11549592 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11549592 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:11549592 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11549592 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11549592 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:11549592 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:11549592 | pubmed:author | pubmed-author:AhmedAA | lld:pubmed |
| pubmed-article:11549592 | pubmed:author | pubmed-author:MasonJJ | lld:pubmed |
| pubmed-article:11549592 | pubmed:author | pubmed-author:DunkCC | lld:pubmed |
| pubmed-article:11549592 | pubmed:author | pubmed-author:KontosC DCD | lld:pubmed |
| pubmed-article:11549592 | pubmed:author | pubmed-author:BussolatiBB | lld:pubmed |
| pubmed-article:11549592 | pubmed:author | pubmed-author:GrohmanMM | lld:pubmed |
| pubmed-article:11549592 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11549592 | pubmed:volume | 159 | lld:pubmed |
| pubmed-article:11549592 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11549592 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11549592 | pubmed:pagination | 993-1008 | lld:pubmed |
| pubmed-article:11549592 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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