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首页> 外文期刊>Journal of Cellular Physiology >Effects of a Sublethal and Transient Stress of the Endoplasmic Reticulum on the Mitochondrial Population
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Effects of a Sublethal and Transient Stress of the Endoplasmic Reticulum on the Mitochondrial Population

机译：亚致死的,瞬态压力的影响内质网在线粒体人口

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Endoplasmic reticulum (ER) and mitochondria are not discrete intracellular organelles but establish close physical and functional interactions involved in several biological processes including mitochondrial bioenergetics, calcium homeostasis, lipid synthesis, and the regulation of apoptotic cell death pathways. As many cell types might face a transient and sublethal ER stress during their lifetime, it is thus likely that the adaptive UPR response might affect the mitochondrial population. The aim of this work was to study the putative effects of a non-lethal and transient endoplasmic reticulum stress on the mitochondrial population in HepG2 cells. The results show that thapsigargin and brefeldin A, used to induce a transient and sublethal ER stress, rapidly lead to the fragmentation of the mitochondrial network associated with a decrease in mitochondrial membrane potential, O2(center dot-) production and less efficient respiration. These changes in mitochondrial function are transient and preceded by the phosphorylation of JNK. Inhibition of JNK activation by SP600125 prevents the decrease in O2(center dot-) production and the mitochondrial network fragmentation observed in cells exposed to the ER stress but has no impact on the reduction of the mitochondrial membrane potential. In conclusion, our data show that a non-lethal and transient ER stress triggers a rapid activation of JNK without inducing apoptosis, leading to the fragmentation of the mitochondrial network and a reduction of O2(center dot-) production. (C) 2015 Wiley Periodicals, Inc.
机译：内质网(ER)和线粒体而不是离散的细胞内的细胞器建立密切的物理和功能相互作用参与多种生物流程包括线粒体生物能疗法,钙稳态、脂质合成,调节凋亡细胞死亡通路。许多细胞类型可能面临一个瞬态和亚致死的一生中ER应激因此可能适应性UPR应答影响线粒体的数量。这项工作研究的假定的影响非致命和瞬态内质网压力对HepG2的线粒体人口细胞。brefeldin,用来产生一个瞬态亚致死的ER应激,迅速导致碎片化的线粒体网络与线粒体减少有关膜电位,O2(中间点)生产和低效率的呼吸。线粒体功能是瞬态和之前物的磷酸化。激活SP600125防止下降O2(中间点)生产和线粒体网络碎片中观察到细胞暴露ER应激但没有影响线粒体膜的减少的潜力。非致命和瞬态压力触发快速激活没有诱导物细胞凋亡,导致的分裂线粒体网络和减少O2(中间点)生产。期刊、公司。

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