Dual phases of respiration chain defect-augmented mROS-mediated mCa 2+ stress during oxidative insult in normal and ρ 0 RBA1 astrocytes.
Dual phases of respiration chain defect-augmented mROS-mediated mCa 2+ stress during oxidative insult in normal and ρ 0 RBA1 astrocytes.
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DOI：
10.1155/2013/159567
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发表时间：
2013
影响因子：
--
通讯作者：
Jou MJ
中科院分区：
文献类型：
--
作者：
Peng TI;Lin MS;Jou MJ
线粒体呼吸链（RC）缺陷导致线粒体ROS （mROS）生成增强，是星形胶质细胞发病机制的基础。然而，据报道，缺乏RC的mtdna缺失细胞（ρ 0）对凋亡敏感或耐药。在这项研究中，我们试图确定氧化损伤后rc增强的线粒体应激的影响。利用无创荧光探针耦合激光扫描成像显微镜，比较了两种不同星形胶质细胞系（对照和ρ 0星形胶质细胞）在氧化应激下抗氧化应激的能力和mROS形成和线粒体钙（mCa2+）的水平。结果表明，RBA-1和ρ 0星形胶质细胞分别在150和130分钟时细胞质膜被YO-PRO-1染料渗透。与RBA-1相比，暴露于20 mM H2O2后30分钟，ρ 0星形胶质细胞形成明显的质膜泡，失去保留Mito-R的能力，细胞核凝结。重要的是，h2o2诱导的ROS和伴随的mCa2+升高在对照组的早期时间点高于ρ 0，而在后期时间点反之亦然。我们的研究结果强调，在短期氧化应激期间，由于RC活性较低，双期RC缺陷细胞具有较少的线粒体应激，但在严重氧化损伤期间，mros介导的mCa2+应激增强。
Mitochondrial respiratory chain (RC) deficits, resulting in augmented mitochondrial ROS (mROS) generation, underlie pathogenesis of astrocytes. However, mtDNA-depleted cells (ρ 0) lacking RC have been reported to be either sensitive or resistant to apoptosis. In this study, we sought to determine the effects of RC-enhanced mitochondrial stress following oxidative insult. Using noninvasive fluorescence probe-coupled laser scanning imaging microscopy, the ability to resist oxidative stress and levels of mROS formation and mitochondrial calcium (mCa2+) were compared between two different astrocyte cell lines, control and ρ 0 astrocytes, over time upon oxidative stress. Our results showed that the cytoplasmic membrane becomes permeated with YO-PRO-1 dye at 150 and 130 minutes in RBA-1 and ρ 0 astrocytes, respectively. In contrast to RBA-1, 30 minutes after 20 mM H2O2 exposure, ρ 0 astrocytes formed marked plasma membrane blebs, lost the ability to retain Mito-R, and showed condensation of nuclei. Importantly, H2O2-induced ROS and accompanied mCa2+ elevation in control showed higher levels than ρ 0 at early time point but vice versa at late time point. Our findings underscore dual phase of RC-defective cells harboring less mitochondrial stress due to low RC activity during short-term oxidative stress but augmented mROS-mediated mCa2+ stress during severe oxidative insult.
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