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线粒体镁离子稳态决定细胞能量代谢及对应激的易感性。

Mitochondrial Mg(2+) homeostasis decides cellular energy metabolism and vulnerability to stress.

作者信息

Yamanaka Ryu, Tabata Sho, Shindo Yutaka, Hotta Kohji, Suzuki Koji, Soga Tomoyoshi, Oka Kotaro

机构信息

Center for Biosciences and Informatics, School of Fundamental Science and Technology Graduate School of Science and Technology, Keio University, Yokohama, 223-8522, Kanagawa, Japan.

Institute for Advanced Biosciences, Keio University, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.

出版信息

Sci Rep. 2016 Jul 26;6:30027. doi: 10.1038/srep30027.

Abstract

Cellular energy production processes are composed of many Mg(2+) dependent enzymatic reactions. In fact, dysregulation of Mg(2+) homeostasis is involved in various cellular malfunctions and diseases. Recently, mitochondria, energy-producing organelles, have been known as major intracellular Mg(2+) stores. Several biological stimuli alter mitochondrial Mg(2+) concentration by intracellular redistribution. However, in living cells, whether mitochondrial Mg(2+) alteration affect cellular energy metabolism remains unclear. Mg(2+) transporter of mitochondrial inner membrane MRS2 is an essential component of mitochondrial Mg(2+) uptake system. Here, we comprehensively analyzed intracellular Mg(2+) levels and energy metabolism in Mrs2 knockdown (KD) cells using fluorescence imaging and metabolome analysis. Dysregulation of mitochondrial Mg(2+) homeostasis disrupted ATP production via shift of mitochondrial energy metabolism and morphology. Moreover, Mrs2 KD sensitized cellular tolerance against cellular stress. These results indicate regulation of mitochondrial Mg(2+) via MRS2 critically decides cellular energy status and cell vulnerability via regulation of mitochondrial Mg(2+) level in response to physiological stimuli.

摘要

细胞能量产生过程由许多依赖镁离子(Mg(2+))的酶促反应组成。事实上,镁离子稳态失调与各种细胞功能障碍和疾病有关。最近,作为产生能量的细胞器,线粒体已被认为是细胞内主要的镁离子储存库。几种生物刺激通过细胞内重新分布改变线粒体镁离子浓度。然而,在活细胞中,线粒体镁离子的改变是否会影响细胞能量代谢仍不清楚。线粒体内膜的镁离子转运体MRS2是线粒体镁离子摄取系统的重要组成部分。在此,我们使用荧光成像和代谢组分析全面分析了MRS2基因敲低(KD)细胞内的镁离子水平和能量代谢。线粒体镁离子稳态失调通过线粒体能量代谢和形态的改变破坏了ATP的产生。此外,MRS2基因敲低增强了细胞对细胞应激的耐受性。这些结果表明,通过MRS2调节线粒体镁离子水平,通过响应生理刺激调节线粒体镁离子水平,对细胞能量状态和细胞易损性起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee52/4960558/401a451dfd1e/srep30027-f1.jpg

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