Transfer of mitochondria from astrocytes to neurons after stroke.
Transfer of mitochondria from astrocytes to neurons after stroke.
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DOI：
10.1038/nature18928
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发表时间：
2016-07-28
期刊：
影响因子：
64.8
通讯作者：
Lo EH
中科院分区：
文献类型：
--
作者：
Hayakawa K;Esposito E;Wang X;Terasaki Y;Liu Y;Xing C;Ji X;Lo EH
最近，有人提出神经元可以释放受损的线粒体并将其转移到星形胶质细胞进行处理和回收。这种交换线粒体的能力可能代表中枢神经系统（CNS）中细胞间信号传导的潜在模式。在这里，我们证明星形胶质细胞还可以释放进入神经元的功能线粒体。细胞外线粒体颗粒的星形胶质细胞释放是由涉及 CD38/环 ADP 核糖信号传导的钙依赖性机制介导的。小鼠短暂性局灶性脑缺血诱导星形胶质细胞线粒体进入邻近神经元，从而放大细胞生存信号。用 siRNA 抑制 CD38 信号传导会减少细胞外线粒体转移并恶化神经系统结果。这些发现表明神经胶质细胞串扰的新线粒体机制可能有助于中风后的内源性神经保护和神经恢复机制。
Recently, it was suggested that neurons can release and transfer damaged mitochondria to astrocytes for disposal and recycling . This ability to exchange mitochondria may represent a potential mode of cell-cell signaling in the central nervous system (CNS). Here, we show that astrocytes can also release functional mitochondria that enter into neurons. Astrocytic release of extracellular mitochondria particles was mediated by a calcium-dependent mechanism involving CD38/cyclic ADP ribose signaling. Transient focal cerebral ischemia in mice induced astrocytic mitochondria entry to adjacent neurons that amplified cell survival signals. Suppression of CD38 signaling with siRNA reduced extracellular mitochondria transfer and worsened neurological outcomes. These findings suggest a new mitochondrial mechanism of neuroglial crosstalk that may contribute to endogenous neuroprotective and neurorecovery mechanisms after stroke.