Publication | Open Access
Hyperplasia of Lymphatic Vessels in VEGF-C Transgenic Mice
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Citations
22
References
1997
Year
Vegf Receptors Vegfr-3ImmunologyPathologyDermatologyVegf-c Transgenic MiceInflammationVascular PermeabilityAngiogenesisLymphatic SystemCell TransplantationAutoimmune DiseaseAutoimmunityVascular BiologyNeovascularizationSclerodermaVascular Endothelial Growth FactorTumor MicroenvironmentDevelopmental BiologyGrowth FactorsLymphatic DiseaseMedicine
Lymphatic vessels lack known specific growth factors, and although VEGF regulates vascular permeability and angiogenesis, it does not stimulate lymphangiogenesis. Transgenic overexpression of VEGF‑C in mouse skin caused selective lymphatic endothelial proliferation and vessel enlargement, indicating that VEGF‑C drives lymphatic hyperplasia and may be relevant to lymphatic disorders and therapeutic lymphangiogenesis.
No growth factors specific for the lymphatic vascular system have yet been described. Vascular endothelial growth factor (VEGF) regulates vascular permeability and angiogenesis, but does not promote lymphangiogenesis. Overexpression of VEGF-C, a ligand of the VEGF receptors VEGFR-3 and VEGFR-2, in the skin of transgenic mice resulted in lymphatic, but not vascular, endothelial proliferation and vessel enlargement. Thus, VEGF-C induces selective hyperplasia of the lymphatic vasculature, which is involved in the draining of interstitial fluid and in immune function, inflammation, and tumor metastasis. VEGF-C may play a role in disorders involving the lymphatic system and may be of potential use in therapeutic lymphangiogenesis.
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