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首页> 外文期刊>Journal of Cellular Physiology >Downregulation of catalase by reactive oxygen species via PI 3 kinase/Akt signaling in mesangial cells.
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Downregulation of catalase by reactive oxygen species via PI 3 kinase/Akt signaling in mesangial cells.

机译：Downregulation活性氧的过氧化氢酶物种通过π3激酶/ Akt信号系膜细胞。

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Reactive oxygen species (ROS) contribute to many glomerular diseases by targeting mesangial cells. ROS have been shown to regulate expression of many antioxidant enzymes including catalase. The mechanism by which the expression of catalase protein is regulated by ROS is not precisely known. Here we report that increased intracellular ROS level by hydrogen peroxide (H(2)O(2)) reduced the expression of catalase. H(2)O(2) increased phosphorylation of Akt kinase in a dose-dependent and sustained manner with a concomitant increase in the phosphorylation of FoxO1 transcription factor. Further analysis revealed that H(2)O(2) promoted rapid activation of phosphatidylinositol (PI) 3 kinase. The PI 3 kinase inhibitor Ly294002 and expression of tumor suppressor protein PTEN inhibited Akt kinase activity, resulting in the attenuation of FoxO1 phosphorylation and preventing the downregulating effect of H(2)O(2) on catalase protein level. Dominant negative Akt attenuated the inhibitory effect of H(2)O(2) on expression of catalase. Constitutively active FoxO1 increased the expression of catalase. However, dominant negative FoxO1 inhibited catalase protein level. Catalase transcription was reduced by H(2)O(2) treatment. Furthermore, expression of dominant negative Akt and constitutively active FoxO1 increased catalase transcription, respectively. These results demonstrate that ROS downregulate the expression of catalase in mesangial cells by PI 3 kinase/Akt signaling via FoxO1 as a target.
机译：活性氧(ROS)导致许多肾小球疾病的目标系膜细胞。ROS已被证明规范的表达许多抗氧化酶包括过氧化氢酶。过氧化氢酶的表达机制蛋白质是由活性氧并不精确已知的。细胞内ROS水平由过氧化氢(H (2) O(2))降低了过氧化氢酶的表达。H (2) O(2)增加一种蛋白激酶激酶的磷酸化在存在剂量依赖的相关性和持续的方式伴随增加的磷酸化FoxO1转录因子。显示H (2) O(2)促进快速激活磷脂酰肌醇(PI) 3激酶。激酶抑制剂Ly294002和表达的肿瘤抑制蛋白PTEN抑制一种蛋白激酶激酶活动,导致FoxO1的衰减磷酸化和防止表达下调影响H (2) O(2)过氧化氢酶蛋白水平。占主导地位的消极Akt减毒的抑制影响H (2) O(2)过氧化氢酶的表达。持续活跃FoxO1增加了过氧化氢酶的表达。负FoxO1抑制过氧化氢酶蛋白水平。过氧化氢酶转录降低了H (2) O (2)治疗。消极的一种蛋白激酶,FoxO1持续活跃分别增加过氧化氢酶转录。这些结果表明,活性氧表达下调系膜细胞中过氧化氢酶的表达通过FoxO1π3激酶/ Akt信号作为目标。

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