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Vasohibin induces prolyl hydroxylase-mediated degradation of hypoxia-inducible factor-1α in human umbilical vein endothelial cells.


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.


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  • Authors

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


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


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

    Pub Type(s)

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



    PubMed ID