Angiostatin induces endothelial cell apoptosis and activation of focal adhesion kinase independently of the integrin-binding motif RGD
Angiostatin induces endothelial cell apoptosis and activation of focal adhesion kinase independently of the integrin-binding motif RGD
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DOI：
10.1073/pnas.95.10.5579
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发表时间：
1998-05-12
影响因子：
11.1
通讯作者：
Folkman, J
中科院分区：
文献类型：
--
作者：
Claesson-Welsh, L;Welsh, M;Folkman, J
血管抑素是纤溶酶原片段，已被鉴定为内源性新生血管抑制因子。我们发现，在没有生长因子的情况下，血管抑素处理内皮细胞会导致凋亡指数增加，而增殖指数没有变化。血管抑素还抑制内皮细胞的迁移和管状形成。Angiostatin对生长因子诱导的信号转导无影响，但可非依赖RGD诱导粘着斑激酶的活性，提示Angiostatin的生物学作用与逆转内皮细胞黏附斑块的形成有关。
Angiostatin, a fragment of plasminogen, has been identified and characterized as an endogenous inhibitor of neovascularization. We show that angiostatin treatment of endothelial cells in the absence of growth factors results in an increased apoptotic index whereas the proliferation index is unchanged. Angiostatin also inhibits migration and tube formation of endothelial cells. Angiostatin treatment has no effect on growth factor-induced signal transduction but leads to an RGD-independent induction of the kinase activity of focal adhesion kinase, suggesting that the biological effects of angiostatin relate to subversion of adhesion plaque formation in endothelial cells.