线粒体复合物 III ROS 调节脂肪细胞分化。
Mitochondrial complex III ROS regulate adipocyte differentiation.
机构信息
Division of Pulmonary and Critical Care, Department of Medicine, Northwestern University Medical School, Chicago, IL 60611, USA.
出版信息
Cell Metab. 2011 Oct 5;14(4):537-44. doi: 10.1016/j.cmet.2011.08.007.
Adipocyte differentiation is characterized by an increase in mitochondrial metabolism. However, it is not known whether the increase in mitochondrial metabolism is essential for differentiation or a byproduct of the differentiation process. Here, we report that primary human mesenchymal stem cells undergoing differentiation into adipocytes display an early increase in mitochondrial metabolism, biogenesis, and reactive oxygen species (ROS) generation. This early increase in mitochondrial metabolism and ROS generation was dependent on mTORC1 signaling. Mitochondrial-targeted antioxidants inhibited adipocyte differentiation, which was rescued by the addition of exogenous hydrogen peroxide. Genetic manipulation of mitochondrial complex III revealed that ROS generated from this complex is required to initiate adipocyte differentiation. These results indicate that mitochondrial metabolism and ROS generation are not simply a consequence of differentiation but are a causal factor in promoting adipocyte differentiation.
脂肪细胞分化的特征是线粒体代谢增加。然而，目前尚不清楚线粒体代谢的增加对于分化是否是必需的，还是分化过程的副产物。在这里，我们报告说，正在分化为脂肪细胞的原代人骨髓间充质干细胞表现出线粒体代谢、生物发生和活性氧（ROS）生成的早期增加。这种早期的线粒体代谢和 ROS 生成的增加依赖于 mTORC1 信号通路。线粒体靶向抗氧化剂抑制脂肪细胞分化，而过氧化氢的添加可挽救这一过程。线粒体复合物 III 的遗传操作表明，该复合物产生的 ROS 对于启动脂肪细胞分化是必需的。这些结果表明，线粒体代谢和 ROS 的产生不是分化的简单结果，而是促进脂肪细胞分化的一个因果因素。
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