Hemangiopoietin promotes endothelial cell proliferation through PI-3K/Akt pathway
Hemangiopoietin promotes endothelial cell proliferation through PI-3K/Akt pathway
复制标题
血管生成素通过 PI-3K/Akt 通路促进内皮细胞增殖
DOI：
10.1159/000149809
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发表时间：
2008-01-01
影响因子：
--
通讯作者：
Han, Zhongchao
中科院分区：
文献类型：
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作者：
Chen, Zhong;Liu, Fang;Han, Zhongchao
血管生成素（HAPO）是一种新型的人生长因子，作用于造血细胞和内皮细胞的原始细胞。我们之前的研究表明，HAPO对内皮细胞具有增殖作用。然而，这种作用的机制尚不清楚。因此，我们研究了HAPO促进人脐静脉内皮细胞（HUVECs）细胞增殖的信号转导途径。在本研究中，重组人HAPO （rhHAPO）以剂量依赖的方式刺激HUVECs的增殖。在HUVECs中加入rhHAPO后，Akt发生了短暂磷酸化。PI-3K特异性抑制剂LY294002显著抑制Akt磷酸化，完全消除hapo刺激的HUVECs增殖。rhHAPO增强cyclin D1的表达，LY294002抑制cyclin D1的上调。此外，rhHAPO能够选择性地增强血管内皮细胞中VEGF的有丝分裂活性。总之，这些发现表明HAPO通过PI-3K/Akt通路诱导内皮细胞增殖。版权所有2008 S. Karger AG，巴塞尔
Hemangiopoietin (HAPO) is a novel human growth factor acting on the primitive cells of both hematopoietic and endothelial cell lineages. Our previous study has shown that HAPO exerts a proliferative effect on endothelial cells. However, the mechanism of this action remains unclear. Thus, we studied the signal transduction pathway whereby HAPO promotes cell proliferation in human umbilical vein endothelial cells (HUVECs). In this study, recombinant human HAPO (rhHAPO) stimulated the proliferation of HUVECs in a dose-dependent manner. The transient phosphorylation of Akt occurred after addition of rhHAPO to HUVECs. LY294002, a specific inhibitor of PI-3K, significantly inhibited Akt phosphorylation and completely abrogated HAPO-stimulated proliferation of HUVECs. rhHAPO enhanced the expression of cyclin D1, where as LY294002 inhibited the up-regulation of cyclin D1. Moreover, rhHAPO is able to selectively enhance the mitogenic activity of VEGF for vascular endothelial cells. Overall, these findings demonstrate that HAPO induces endothelial cell proliferation through the PI-3K/Akt pathway. Copyright (C) 2008 S. Karger AG, Basel.