Copper chelator ATN-224 inhibits endothelial function by multiple mechanisms
Copper chelator ATN-224 inhibits endothelial function by multiple mechanisms
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DOI：
10.1016/j.mvr.2009.01.003
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发表时间：
2009-05-01
影响因子：
3.1
通讯作者：
Harris, Adrian L.
中科院分区：
文献类型：
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作者：
Lowndes, Sarah A.;Sheldon, Helen V.;Harris, Adrian L.
内皮细胞的增殖需要铜，降铜疗法可减少动物模型中肿瘤的生长。据报道，新型铜螯合剂 ATN-224 能有效抑制内皮细胞中依赖铜的超氧化物歧化酶 I（SOD1）的活性。我们对暴露于 ATN-224 的内皮细胞的基因表达进行了微阵列分析，结果显示应激反应基因（包括血红素氧化酶 1 (HO-1)）的上调，以及先前与血管生成有关的几个基因（包括 CXCR4、ANGP2、PGES2、RHAMM、ITB4 和 AQP1）的不同调控（p＜0.05）。
Copper is required for the proliferation of endothelial cells and copper-lowering therapy reduces tumour growth in animal models. It has been reported that ATN-224, a novel copper chelator, potently inhibits the activity of the copper-dependent enzyme superoxide dismutase I (SOD1) in endothelial cells. We performed microarray analysis of gene expression in endothelial cells exposed to ATN-224 which revealed upregulation of stress response genes including heme-oxygenase 1 (HO-1) and differential regulation of several genes previously implicated in angiogenesis including CXCR4, ANGP2, PGES2, RHAMM, ITB4 and AQP1 (p