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首页> 外文期刊>Cellular Physiology and Biochemistry >NOX2, p22phox and p47phox are Targeted to the Nuclear Pore Complex in Ischemic Cardiomyocytes Colocalizing with Local Reactive Oxygen Species
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NOX2, p22phox and p47phox are Targeted to the Nuclear Pore Complex in Ischemic Cardiomyocytes Colocalizing with Local Reactive Oxygen Species

机译：NOX2，p22phox和p47phox定位于局部活性氧物种共定位的局部缺血心肌细胞中的核孔复合体

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Background NADPH oxidases play an essential role in reactive oxygen species (ROS)-based signaling in the heart. Previously, we have demonstrated that (peri)nuclear expression of the catalytic NADPH oxidase subunit NOX2 in stressed cardiomyocytes, e.g. under ischemia or high concentrations of homocysteine, is an important step in the induction of apoptosis in these cells. Here this ischemia-induced nuclear targeting and activation of NOX2 was specified in cardiomyocytes. Methods The effect of ischemia, mimicked by metabolic inhibition, on nuclear localization of NOX2 and the NADPH oxidase subunits p22supphox/sup and p47supphox/sup, was analyzed in rat neonatal cardiomyoblasts (H9c2 cells) using Western blot, immuno-electron microscopy and digital-imaging microscopy. Results NOX2 expression significantly increased in nuclear fractions of ischemic H9c2 cells. In addition, in these cells NOX2 was found to colocalize in the nuclear envelope with nuclear pore complexes, p22supphox/sup, p47supphox/sup and nitrotyrosine residues, a marker for the generation of ROS. Inhibition of NADPH oxidase activity, with apocynin and DPI, significantly reduced (peri)nuclear expression of nitrotyrosine. Conclusion We for the first time show that NOX2, p22supphox/sup and p47supphox/sup are targeted to and produce ROS at the nuclear pore complex in ischemic cardiomyocytes.
机译：背景NADPH氧化酶在心脏中基于活性氧（ROS）的信号传导中起重要作用。先前，我们已经证明了在应激的心肌细胞中，例如催化的NADPH氧化酶亚基NOX2的（周）核表达。在缺血或高半胱氨酸的高浓度下，是诱导这些细胞凋亡的重要步骤。在这里，在心肌细胞中确定了这种缺血诱导的核靶向和NOX2的激活。方法通过代谢抑制模拟缺血对大鼠新生心肌细胞（H9c2细胞）中NOX2和NADPH氧化酶亚基p22 phox 和p47 phox 的核定位的影响），使用Western印迹，免疫电子显微镜和数字成像显微镜。结果缺血的H​​9c2细胞的核级分中NOX2表达显着增加。此外，在这些细胞中，发现NOX2与核孔复合物p22 phox ，p47 phox 和硝基酪氨酸残基共定位于核被膜中，后者是产生ROS的标记。载有Apocynin和DPI抑制NADPH氧化酶活性，显着降低了硝基酪氨酸的（核）核表达。结论我们首次表明，NOX2，p22 phox 和p47 phox 被靶向并在缺血性心肌细胞的核孔复合物中产生ROS。

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