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

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• 作者：Tomohiro Kozako^a ; Noriko Matsumoto^a ; Yukako Kuramoto^a ; Akira Sakata^b ; Rie Motonagare^a ; Akiyoshi Aikawa^a ; Masumi Imoto^c ; Akihisa Toda^c ; Shin-ichiro Honda^a ; Hiroshi Shimeno^a ; Shinji Soeda^a ; ^{ssoeda@fukuoka-u.ac.jp}
• 关键词：H2O2 ; hydrogen peroxide ; HIF-1伪 ; hypoxia-inducible factor-1伪 ; HUVEC ; human umbilical vein endothelial cells ; PHD ; prolyl hydroxylase ; ROS ; reactive oxygen species ; VEGF ; vascular endothelial growth factor ; VHL ; von Hippel&ndash ; Lindau (VHL)
• 刊名：FEBS Letters
• 出版年：2012
• 期刊代码：70_00145793
• 类别：bio
• 出版时间：5 April, 2012
• 卷：586
• 期：7
• 页码：1067-1072
• 文件大小：1017 K

摘要

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-1伪 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-1伪 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-1伪 degradation via PHD.