Open AccessDownregulation of Fes inhibits VEGF‐A‐induced chemotaxis and capillary‐like morphogenesis by cultured endothelial cells
Author(s) -
Kanda Shigeru,
Kanetake Hiroshi,
Miyata Yasuyoshi
Publication year - 2007
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2007.00034.x
Subject(s) - downregulation and upregulation , ly294002 , autophosphorylation , microbiology and biotechnology , chemotaxis , vascular endothelial growth factor , vascular endothelial growth factor a , kinase insert domain receptor , protein kinase b , chemistry , biology , kinase , protein kinase a , phosphorylation , cancer research , receptor , vegf receptors , biochemistry , gene
The aim of this study was to determine whether the downregulation of endogenous Fes by siRNA in cultured endothelial cells affects vascular endothelial growth factor‐A (VEGF‐A)‐induced chemotaxis and capillary‐like morphogenesis, which are considered as angiogenic cellular responses in vitro. VEGF‐A‐treatment induced autophosphorylation of Fes in cultured endothelial cells.LY294002, a phosphoinositide 3‐kinase inhibitor, significantly inhibited VEGF‐A‐induced chemotaxis and capillary‐like morphogenesis.Downregulation of Fes attenuated these VEGF‐A‐induced cellular responses but LY294002 did not produce further inhibition of these responses. Downregulation of Fes neither affected VEGF‐A‐induced autophosphorylation of VEGF receptor 2 nor mitogen‐activated protein kinase activation, but markedly decreased Akt activation.Taken together, our novel results indicate the involvement of Fes in VEGF‐A‐induced cellular responses by cultured endothelial cells.