pubmed-article:11090062 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11090062 | lifeskim:mentions | umls-concept:C0018951 | lld:lifeskim |
pubmed-article:11090062 | lifeskim:mentions | umls-concept:C0388911 | lld:lifeskim |
pubmed-article:11090062 | lifeskim:mentions | umls-concept:C0169539 | lld:lifeskim |
pubmed-article:11090062 | lifeskim:mentions | umls-concept:C0378796 | lld:lifeskim |
pubmed-article:11090062 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
pubmed-article:11090062 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:11090062 | pubmed:dateCreated | 2000-12-11 | lld:pubmed |
pubmed-article:11090062 | pubmed:abstractText | Signaling by vascular endothelial growth factors (VEGFs) through VEGF receptors (VEGFRs) plays important roles in vascular development and hematopoiesis. The authors analyzed the function of VEGF-C signaling through both VEGFR-2 and VEGFR-3 in vasculoangiogenesis and hematopoiesis using a coculture of para-aortic splanchnopleural mesoderm (P-Sp) explants from mouse embryos with stromal cells (OP9). Vasculogenesis and angiogenesis were evaluated by the extent of vascular bed and network formation, respectively. Addition of VEGF-C to the P-Sp culture enhanced vascular bed formation and suppressed definitive hematopoiesis. Both vascular bed and network formations were completely suppressed by addition of soluble VEGFR-1-Fc competitor protein. Formation of vascular beds but not networks could be rescued by VEGF-C in the presence of the competitor, while both were rescued by VEGF-A. VEGFR-3-deficient embryos show the abnormal vasculature and severe anemia. Consistent with these in vivo findings, vascular bed formation in the P-Sp from the VEGFR-3-deficient embryos was enhanced to that in wild-type or heterozygous embryos, and hematopoiesis was severely suppressed. When VEGFR-3-Fc chimeric protein was added to trap endogenous VEGF-C in the P-Sp culture of the VEGFR-3-deficient embryos, vascular bed formation was suppressed and hematopoiesis was partially rescued. These results demonstrate that because VEGF-C signaling through VEGFR-2 works synergistically with VEGF-A, the binding of VEGF-C to VEGFR-3 consequently regulates VEGFR-2 signaling. In VEGFR-3-deficient embryos, an excess of VEGF-C signals through VEGFR-2 induced the disturbance of vasculogenesis and hematopoiesis during embryogenesis. This indicates that elaborated control through VEGFR-3 signaling is critical in vasculoangiogenesis and hematopoiesis. (Blood. 2000;96:3793-3800) | lld:pubmed |
pubmed-article:11090062 | pubmed:language | eng | lld:pubmed |
pubmed-article:11090062 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11090062 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:11090062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11090062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11090062 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11090062 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11090062 | pubmed:month | Dec | lld:pubmed |
pubmed-article:11090062 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:ItoYY | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:SudaTT | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:HamadaKK | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:AlitaloKK | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:OikeYY | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:TakakuraNN | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:DumontD JDJ | lld:pubmed |
pubmed-article:11090062 | pubmed:author | pubmed-author:JussilaLL | lld:pubmed |
pubmed-article:11090062 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11090062 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11090062 | pubmed:volume | 96 | lld:pubmed |
pubmed-article:11090062 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11090062 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11090062 | pubmed:pagination | 3793-800 | lld:pubmed |
pubmed-article:11090062 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:11090062 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:11090062 | pubmed:articleTitle | VEGF-C signaling pathways through VEGFR-2 and VEGFR-3 in vasculoangiogenesis and hematopoiesis. | lld:pubmed |
pubmed-article:11090062 | pubmed:affiliation | Department of Cell Differentiation, Institute of Molecular Embryology and Genetics, Kumamoto University, Japan. | lld:pubmed |
pubmed-article:11090062 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11090062 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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