title: Vasohibin induces prolyl hydroxylase-mediated degradation of hypoxia-inducible factor-1α in human umbilical vein endothelial cells.
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.
authors.affiliation: Department of Biochemistry, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Kozako
authors.forename: Noriko
authors.initials: N
authors.lastname: Matsumoto
authors.forename: Yukako
authors.initials: Y
authors.lastname: Kuramoto
authors.forename: Akira
authors.initials: A
authors.lastname: Sakata
authors.forename: Rie
authors.initials: R
authors.lastname: Motonagare
authors.forename: Akiyoshi
authors.initials: A
authors.lastname: Aikawa
authors.forename: Masumi
authors.initials: M
authors.lastname: Imoto
authors.forename: Akihisa
authors.initials: A
authors.lastname: Toda
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Honda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Shimeno
authors.forename: Shinji
authors.initials: S
authors.lastname: Soeda
mesh_terms: D001692:Biological Transport / Q000187:drug effects; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D025461:Feedback, Physiological; D005786:Gene Expression Regulation / Q000187:drug effects; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects / Q000201:enzymology* / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism*; D007527:Isoenzymes / Q000378:metabolism; D009389:Neovascularization, Pathologic / Q000517:prevention & control; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress; D011393:Procollagen-Proline Dioxygenase / Q000378:metabolism*; D059748:Proteolysis / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D007527:Isoenzymes; D016877:Oxidants; D012333:RNA, Messenger; D011994:Recombinant Proteins; C493181:VASH1 protein, human; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D006861:Hydrogen Peroxide; D011393:Procollagen-Proline Dioxygenase