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Hyperplasia of lymphatic vessels in VEGF-C transgenic mice

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Publication Date
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Infoscience @ EPFL
Keywords
  • Animals
  • Cell Division
  • Cloning
  • Molecular
  • Endothelial Growth Factors/Genetics/*Physiology
  • Endothelium
  • Lymphatic/Physiology/Ultrastructure
  • Endothelium
  • Vascular/Physiology
  • Humans
  • Hyperplasia
  • Immunohistochemistry
  • In Situ Hybridization
  • Lymphatic System/*Pathology
  • Mice
  • Mice
  • Inbred C57Bl
  • Mice
  • Inbred Dba
  • Mice
  • Transgenic
  • Molecular Sequence Data
  • Rna
  • Messenger/Metabolism
  • Receptor Protein-Tyrosine Kinases/Metabolism
  • Receptors
  • Cell Surface/Metabolism
  • Receptors
  • Growth Factor/Metabolism
  • Receptors
  • Vascular Endothelial Growth Factor
  • Skin/Pathology
  • Vascular Endothelial Growth Factor C
  • Vascular Endothelial Growth Factor Receptor-3
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Abstract

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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