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首页> 外文期刊>Molecular and Cellular Biology >Oxidative Stress-Responsive Transcription Factor ATF3 Potentially Mediates Diabetic Angiopathy
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Oxidative Stress-Responsive Transcription Factor ATF3 Potentially Mediates Diabetic Angiopathy

机译：氧化应激反应转录因子ATF3可能介导糖尿病血管病。

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Previous results of our cDNA microarray analysis to look for genes whose expression level correlates well with in vitro tubulogenesis by NP31 endothelial cells revealed the transcription factor ATF3 known to be responsive to stress such as reactive oxygen species (ROS). Anti-ATF3 small interfering RNA gave an inhibitory influence on tube formation by NP31 cells expressing an activated form of the vascular endothelial growth factor receptor 1 (VEGFR-1) kinase. When expression of ATF3 was regulated under the control of tetracycline system in NP31 cells, they acquired the tubulogenic ability upon ATF3 induction. While ATF3 failed to induce expressions of VEGF and VEGFR, it regulated those of CDK2, CDK4, p8, plasminogen activator inhibitor 1, integrin α1, subunit and matrix metalloprotease MMP13. In H2O2-stimulated NP31 cells as well as endothelial cells of glomerulus and aorta of Otsuka-Long-Evans-Tokushima-Fatty diabetic model rats, concomitantly enhanced expressions of ATF3, PAI-1, and p8 were observed. Given the proposed hypothesis of the close linkage between diabetic angiopathy and ROS, those data suggest that ROS-associated diabetic complication may involve ATF3-mediated pathological angiogenesis.
机译：我们的cDNA微阵列分析以前的结果来寻找其表达水平与NP31内皮细胞体外微管发生密切相关的基因，揭示了转录因子ATF3已知对压力（例如活性氧（ROS））有反应。抗ATF3小干扰RNA对表达血管内皮生长因子受体1（VEGFR-1）激酶活化形式的NP31细胞的管形成产生抑制作用。当在四环素系统的控制下，NP31细胞中ATF3的表达受到调节时，它们在ATF3诱导后获得了促成血管的能力。尽管ATF3无法诱导VEGF和VEGFR的表达，但它调节了CDK2，CDK4，p8，纤溶酶原激活物抑制剂1，整合素α1，亚基和基质金属蛋白酶MMP13的表达。在H 2 O 2 刺激的大冢-朗-伊文斯-德岛-胖子糖尿病模型大鼠的肾小球和主动脉的NP31细胞以及肾小球和内皮细胞中，观察到ATF3，PAI-1和p8。考虑到所提出的糖尿病性血管病与ROS之间紧密联系的假说，这些数据表明ROS相关的糖尿病并发症可能涉及ATF3介导的病理性血管生成。

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