Premium
Vasohibin induces prolyl hydroxylase‐mediated degradation of hypoxia‐inducible factor‐1α in human umbilical vein endothelial cells
Author(s) -
Kozako Tomohiro,
Matsumoto Noriko,
Kuramoto Yukako,
Sakata Akira,
Motonagare Rie,
Aikawa Akiyoshi,
Imoto Masumi,
Toda Akihisa,
Honda Shin-ichiro,
Shimeno Hiroshi,
Soeda Shinji
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.03.007
Subject(s) - angiogenesis , umbilical vein , chemistry , vascular endothelial growth factor , oxidative stress , cell growth , hypoxia inducible factors , regulator , human umbilical vein endothelial cell , hypoxia (environmental) , microbiology and biotechnology , biochemistry , vegf receptors , cancer research , biology , oxygen , organic chemistry , gene , in vitro
Vasohibin is thought to be an important negative feedback regulator of angiogenesis that is selectively induced in endothelial cells by VEGF. Here, we assessed the role of vasohibin on HIF‐1α expression under oxidative stress induced by hydrogen peroxide (H 2 O 2 ) in HUVEC. VEGF induced significant cell growth that was associated with an increase in vasohibin expression. Following H 2 O 2 ‐pretreatment, VEGF further increased cell growth but this was contrastingly associated with a decrease in vasohibin expression when compared with VEGF alone. Interestingly, vasohibin inhibited cell proliferation through degradation of HIF‐1α expression during H 2 O 2 ‐pretreatment. Furthermore, vasohibin elevated the expression of prolyl hydroxylase (PHD). These results suggest that vasohibin plays crucial roles as a negative feedback regulator of angiogenesis through HIF‐1α degradation via PHD.