Abstract

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 (H₂O₂) in HUVEC. VEGF induced significant cell growth that was associated with an increase in vasohibin expression. Following H₂O₂-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 H₂O₂-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.

Links

Publisher Full Text

Authors

Kozako T, Matsumoto N, Kuramoto Y, Sakata A, Motonagare R, Aikawa A, Imoto M, Toda A, Honda S, Shimeno H, Soeda S

Institution

Department of Biochemistry, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.

Source

FEBS letters 586:7 2012 Apr 5 pg 1067-72

MeSH

Biological Transport
Cell Cycle Proteins
Cell Nucleus
Cell Proliferation
Cells, Cultured
Feedback, Physiological
Gene Expression Regulation
Human Umbilical Vein Endothelial Cells
Humans
Hydrogen Peroxide
Hypoxia-Inducible Factor 1, alpha Subunit
Isoenzymes
Neovascularization, Pathologic
Oxidants
Oxidative Stress
Procollagen-Proline Dioxygenase
Proteolysis
RNA, Messenger
Recombinant Proteins
Vascular Endothelial Growth Factor A

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22569265