| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2047873 | FEBS Letters | 2012 | 6 Pages |
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.
► H2O2-pretreatment before VEGF stimulation increased cell growth. ► H2O2-pretreatment before VEGF stimulation decreased vasohibin expression. ► H2O2-mediated degradation of vasohibin protein and mRNA was dose-dependent. ► Vasohibin inhibited cell proliferation through the degradation of HIF-1α expression. ► Vasohibin elevated the expression of PHD, which regulates HIF hydroxylation.
