| pubmed-article:16453023 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0175677 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0078058 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0378516 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0596087 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:16453023 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
| pubmed-article:16453023 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:16453023 | pubmed:dateCreated | 2006-2-2 | lld:pubmed |
| pubmed-article:16453023 | pubmed:abstractText | VEGF-A promotes angiogenesis in many tissues. Here we report that choroidal neovascularization (CNV) incited by injury was increased by excess VEGF-A before injury but was suppressed by VEGF-A after injury. This unorthodox antiangiogenic effect was mediated via VEGFR-1 activation and VEGFR-2 deactivation, the latter via Src homology domain 2-containing (SH2-containing) tyrosine phosphatase-1 (SHP-1). The VEGFR-1-specific ligand placental growth factor-1 (PlGF-1), but not VEGF-E, which selectively binds VEGFR-2, mimicked these responses. Excess VEGF-A increased CNV before injury because VEGFR-1 activation was silenced by secreted protein, acidic and rich in cysteine (SPARC). The transient decline of SPARC after injury revealed a temporal window in which VEGF-A signaling was routed principally through VEGFR-1. These observations indicate that therapeutic design of VEGF-A inhibition should include consideration of the level and activity of SPARC. | lld:pubmed |
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| pubmed-article:16453023 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16453023 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16453023 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16453023 | pubmed:month | Feb | lld:pubmed |
