Laboratory of Molecular Biochemistry, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo 192-0392, Japan.
Biomolecules. 2020 Mar 13;10(3):0. doi: 10.3390/biom10030450.
Mitochondria are highly dynamic organelles that constantly fuse, divide, and move, and their function is regulated and maintained by their morphologic changes. Mitochondrial disease (MD) comprises a group of disorders involving mitochondrial dysfunction. However, it is not clear whether changes in mitochondrial morphology are related to MD. In this study, we examined mitochondrial morphology in fibroblasts from patients with MD (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) and Leigh syndrome). We observed that MD fibroblasts exhibited significant mitochondrial fragmentation by upregulation of Drp1, which is responsible for mitochondrial fission. Interestingly, the inhibition of mitochondrial fragmentation by Drp1 knockdown enhanced cellular toxicity and led to cell death in MD fibroblasts. These results suggest that mitochondrial fission plays a critical role in the attenuation of mitochondrial damage in MD fibroblasts.
线粒体是高度动态的细胞器,不断融合、分裂和移动,其功能通过形态变化来调节和维持。线粒体疾病(MD)包括一组涉及线粒体功能障碍的疾病。然而,线粒体形态的变化是否与 MD 有关尚不清楚。在这项研究中,我们研究了 MD(线粒体肌病、脑病、乳酸酸中毒和卒中样发作(MELAS)和 Leigh 综合征)患者成纤维细胞中的线粒体形态。我们观察到,由于 Drp1 的上调,导致线粒体分裂的 MD 成纤维细胞表现出明显的线粒体碎片化。有趣的是,Drp1 敲低抑制线粒体碎片化会增强细胞毒性,并导致 MD 成纤维细胞死亡。这些结果表明,线粒体分裂在 MD 成纤维细胞中线粒体损伤的减轻中起着关键作用。