组蛋白去乙酰化酶3作为血管生成的负调控因子。
HDAC3 acts as a negative regulator of angiogenesis.
作者信息
Park Deokbum, Park Hyunmi, Kim Youngmi, Kim Hyuna, Jeoung Dooil
机构信息
Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon 200-701, Korea.
出版信息
BMB Rep. 2014 Apr;47(4):227-32. doi: 10.5483/bmbrep.2014.47.4.128.
Histone deacetylase-3 (HDAC3) is involved in cellular proliferation, apoptosis and transcriptional repression. However, the role of HDAC3 in angiogenesis remains unknown. HDAC3 negatively regulated the expression of angiogenic factors, such as VEGF and plasminogen activator inhibitor-1 (PAI-1). HDAC3 showed binding to promoter sequences of PAI-1. HDAC3 activity was necessary for the expression regulation of PAI-1 by HDAC3. VEGF decreased the expression of HDAC3, and the down-regulation of HDAC3 enhanced endothelial cell tube formation. HDAC3 negatively regulated tumor-induced angiogenic potential. We show the novel role of HDAC3 as a negative regulator of angiogenesis.
组蛋白去乙酰化酶3（HDAC3）参与细胞增殖、凋亡及转录抑制。然而，HDAC3在血管生成中的作用尚不清楚。HDAC3负向调节血管生成因子如血管内皮生长因子（VEGF）和纤溶酶原激活物抑制剂1（PAI-1）的表达。HDAC3显示与PAI-1的启动子序列结合。HDAC3活性对于HDAC3对PAI-1的表达调控是必需的。VEGF降低HDAC3的表达，而HDAC3的下调增强内皮细胞管腔形成。HDAC3负向调节肿瘤诱导的血管生成潜能。我们揭示了HDAC3作为血管生成负调节因子的新作用。
Zotero 插件