Vascular endothelial growth factor C is required for sprouting of the first lymphatic vessels from embryonic veins
By M. Karkkainen, P. Haiko, K. Sainio, J. Partanen, Jussi Taipale, T. Petrova, M. Jeltsch, D. Jackson, M. Talikka, H. Rauvala and 2 more. Nature Immunology, 2004
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Subfields: Cell Biology, Oncology, Physiology
View Paper: https://www.semanticscholar.org/paper/400d8b4ebbb5a9f7f28eda3ed1a9fa06e1de5e06
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Citations in the corpus
- Lymphangiogenesis: Molecular mechanisms and future promise. (2010, background): “In mice, Xenopus tadpoles, and zebrafish where Vegfc has been inactivated, LECs initially differentiate in the embryonic veins but fail to migrate and form the primary lymph sacs (Karkkainen et al., 2004; Kuchler et al., 2006; Yaniv et al., 2006).”
- The lymphatic vasculature in disease (2011, background): “The blood vasculature is formed by vasculogenesis and angiogenesis, driven chiefly by vascular endothelial growth factor (VEGF), whereas lymphangiogenesis is induced by VEGF-C, which acts on LECs that differentiate from venous endothelial cells at midgestatio”
- AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer. (2005, background): “This receptor has a critical role in lymphangiogenesis (38) and a prognostic link with expression of VEGF-C and/or VEGF-D and nodal metastasis has been identified for different tumor types (39, 40).”
- Biology of vascular endothelial growth factors (2006, background): “Developmental studies, knockout models and gene transfer experiments suggest that VEGF-C is primarily a lymphangiogenic growth factor and its lymphangiogenic effects are mediated by VEGFR-3 [30,31].”
- CCBE1 Enhances Lymphangiogenesis via A Disintegrin and Metalloprotease With Thrombospondin Motifs-3–Mediated Vascular Endothelial Growth Factor-C Activation (2014, methodology): “Deletion of the Vegfc gene in mice results in failure of lymphatic development because of the inability of newly differentiated lymphatic endothelial cells to migrate from the cardinal veins to sites where the first lymphatic structures form.(2,3) This phenotype could be rescued by the application o”
- Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation. (2005, neutral): “for mouse Vegfc (7) or Vegfd (GenBank accession number NM010216, base”
- Wound repair at a glance (2009, background): “…(repair of lymph vessels) has been studied much less than Journal of Cell Science 122 (18) Jo ur na l o f C el l S ci en ce 3211 angiogenesis, but is likewise under tight regulation by a plethora of similar, as well as some unique, growth factors (Adams and Alitalo, 2007; Karkkainen et al., 2004).”
- Signal transduction by vascular endothelial growth factor receptors. (2012, background): “vein is critical for development of the lymphatic system (Karkkainen et al. 2004).”
- VEGF receptor signalling ? in control of vascular function (2006, background): “5 in response to a gradient of VEGFC, which is produced by nearby mesenchymal cells”
- Vascular endothelial growth factor (VEGF) signaling in tumor progression. (2007, background): “VEGF-C is thus indispensble for embryonic lymphangiogenesis [80].”
- Vascular endothelial growth factor and its receptor system: physiological functions in angiogenesis and pathological roles in various diseases. (2013, background): “VEGF-C, but not VEGF-D, is expressed during embryogenesis, and VEGF-C null mice (VEGF-C / ) exhibit a lethal phenotype at the prenatal stage due to fluid accumulation in tissues because of poor lymphangiogenesis (11).”