Open AccessVascular endothelial growth factor receptor expression during embryogenesis and tissue repair suggests a role in endothelial differentiation and blood vessel growth.
Author(s) -
Kevin G. Peters,
Carlie de Vries,
L T Williams
Publication year - 1993
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.90.19.8915
Subject(s) - biology , vascular endothelial growth factor b , mesenchyme , endothelium , angiogenesis , microbiology and biotechnology , vascular endothelial growth factor , vascular endothelial growth factor c , vascular endothelial growth factor a , neovascularization , blood vessel , vasculogenesis , in situ hybridization , receptor tyrosine kinase , immunology , endocrinology , cancer research , signal transduction , mesenchymal stem cell , stem cell , gene expression , progenitor cell , genetics , vegf receptors , gene
Vascular endothelial growth factor (VEGF) is a polypeptide mitogen that stimulates the growth of endothelial cells in vitro and promotes the growth of blood vessels in vivo. We have recently shown that the fms-like receptor tyrosine kinase (flt) is a receptor for VEGF. Here we used in situ hybridization to show that, in adult mouse tissues, the pattern of flt expression was consistent with localization in endothelium. We also show that flt was expressed in endothelium during neovascularization of healing skin wounds and during early vascular development in mouse embryos. Moreover, flt was expressed in populations of embryonic cells from which endothelium is derived such as early yolk sac mesenchyme. The expression of flt in the endothelium of both developing and mature blood vessels suggests that VEGF might regulate endothelial differentiation, blood vessel growth, and vascular repair.