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Fine-tuning the angiogenic response to vascular endothelial growth factor.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Liao, James K. |
| Copyright Year | 2008 |
| Abstract | See related article, pages 261–268 Vascular endothelial growth factor (VEGF) is an important mediator of vascular development and postnatal angiogenesis.1,2 Homozygous deletion of VEGF gene leads to impaired vascular formation and early embryonic lethality.3 Interestingly, deletion of just one VEGF allele is sufficient to produce similar vascular abnormalities,3,4 suggesting that the strength and integrity of the VEGF signaling pathway are critical for the spatial–temporal formation of blood vessels in utero. These actions of VEGF are mediated predominantly by 2 tyrosine kinase receptors: VEGFR-1 (flt-1) and VEGFR-2 (flk-1/KDR).5 Mice with homozygous mutations that inactivate either receptor die in utero with a similar phenotype as mice with VEGF deletion, indicating that both receptors are obligatory for the function of VEGF.1,6 Although the vascular phenotype between these VEGFR mutant mice are overlapping to some degree, they do differ in terms of showing that VEGFR-2 plays a greater role in vascular organization,7 whereas VEGFR-1 appears to be more important in mediating hemangioblast commitment and endothelial cell replication.8 Nevertheless, both VEGFR-1 and VEGFR-2 are essential in coordinating endothelial cell assembly and vascular formation during embryonic development. The upregulation of VEGF is also necessary for physiological and pathological neovascularization in response to hypoxia and for tumor … |
| Starting Page | 1 |
| Ending Page | 1 |
| Page Count | 1 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://circres.ahajournals.org/content/circresaha/103/3/229.full.pdf?download=true |
| Alternate Webpage(s) | http://circres.ahajournals.org/content/circresaha/103/3/229.full.pdf |
| PubMed reference number | 18669928v1 |
| Alternate Webpage(s) | https://doi.org/10.1161/CIRCRESAHA.108.181628 |
| DOI | 10.1161/circresaha.108.181628 |
| Journal | Circulation research |
| Volume Number | 103 |
| Issue Number | 3 |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Activation action American Heart Association Angiogenic Process Aorta Blood Vessel Cardiovascular Diseases Cell Culture Techniques Cell Proliferation Circumference Cross Reactions Cross-Talk Cyclic GMP Deletion Mutation Email Embryonic Development Endothelial Cells Endothelial Growth Factors FLT1 protein, human FLT1 wt Allele Heart valve disease Hemangioblasts Homozygote Hypoxia Hypoxia-Ischemia, Brain Ischemia Lower Extremity Mediator brand of benfluorex hydrochloride NOS3 gene NOS3 protein, human Neoplasms Nitric Oxide Synthase Non-Small Cell Lung Carcinoma Pathologic Neovascularization Placenta Promotion (action) Protein Tyrosine Kinase Proto-Oncogene Proteins c-akt RNA Receptor Protein-Tyrosine Kinases Recombinant Vascular Endothelial Growth Factor Retroviridae Signal Transduction Pathways Tissue membrane Tyrosine Kinase Domain Uterus Vascular Endothelial Growth Factor Receptor 2, human Vascular Endothelial Growth Factor Receptor-1 Vascular Endothelial Growth Factor Receptor-2 Vascular Medicine Wild Type Unspecified - zebrafish bevacizumab negative regulation of vascular endothelial growth factor signaling pathway protein expression |
| Content Type | Text |
| Resource Type | Article |
