Inostamycin suppresses vascular endothelial growth factor-stimulated growth and migration of human umbilical vein endothelial cells.
Angiogenesis involves multiple steps including proliferation and migration of endothelial cells. In the present study, we determined the effect of inostamycin (an inhibitor of phosphatidylinositol synthesis) on vascular endothelial growth factor (VEGF)-induced proliferation and migration of human umbilical vein endothelial cells (HUVECs). Inostamycin significantly attenuated both VEGF-induced proliferation and migration of HUVECs. Inostamycin inhibited activation of mitogen-activated kinases (ERK and p38) and elevation of cyclin D1 induced by VEGF. These data suggest that inostamycin reduced both proliferation and migration of HUVECs by targeting ERK-cyclin D1 and p38, respectively.
Baba
Yuh
Y
Department of Biology and Function in the Head and Neck, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Kato
Yasumasa
Y
Mochimatsu
Izumi
I
Nagashima
Yoji
Y
Kurihara
Miki
M
Kawano
Toshiro
T
Taguchi
Takahide
T
Hata
Ryu-Ichiro
R
Tsukuda
Mamoru
M
D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D019938:Cyclin D1 / Q000494:pharmacology; D042783:Endothelial Cells / Q000187:drug effects*; D005663:Furans / Q000494:pharmacology*; D006801:Humans; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D014471:Umbilical Veins / Q000187:drug effects*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism / Q000494:pharmacology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D005663:Furans; D042461:Vascular Endothelial Growth Factor A; C071861:inostamycin; D019938:Cyclin D1; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases