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局部糖酵解支持损伤诱导的轴突再生。

Local glycolysis supports injury-induced axonal regeneration.

机构信息

Department of Biology, Animal Physiology and Neurobiology Section, KU Leuven, Leuven Brain Institute, Leuven, Belgium.

Neuro-Electronics Research Flanders, Vlaams Instituut voor Biotechnologie , Leuven, Belgium.

出版信息

J Cell Biol. 2024 Dec 2;223(12). doi: 10.1083/jcb.202402133. Epub 2024 Oct 1.

DOI:10.1083/jcb.202402133
PMID:39352499
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11451009/
Abstract

Successful axonal regeneration following injury requires the effective allocation of energy. How axons withstand the initial disruption in mitochondrial energy production caused by the injury and subsequently initiate regrowth is poorly understood. Transcriptomic data showed increased expression of glycolytic genes after optic nerve crush in retinal ganglion cells with the co-deletion of Pten and Socs3. Using retinal cultures in a multicompartment microfluidic device, we observed increased regrowth and enhanced mitochondrial trafficking in the axons of Pten and Socs3 co-deleted neurons. While wild-type axons relied on mitochondrial metabolism, after injury, in the absence of Pten and Socs3, energy production was supported by local glycolysis. Specific inhibition of lactate production hindered injury survival and the initiation of regrowth while slowing down glycolysis upstream impaired regrowth initiation, axonal elongation, and energy production. Together, these observations reveal that glycolytic ATP, combined with sustained mitochondrial transport, is essential for injury-induced axonal regrowth, providing new insights into the metabolic underpinnings of axonal regeneration.

摘要

轴突再生需要有效的能量分配。轴突如何在损伤引起的线粒体能量产生最初中断后承受并随后启动再生，目前还知之甚少。转录组数据显示，在视网膜神经节细胞中敲除 Pten 和 Socs3 后，视神经挤压后糖酵解基因的表达增加。使用多隔室微流控装置中的视网膜培养物，我们观察到 Pten 和 Socs3 共同缺失神经元的轴突中再生增加和线粒体运输增强。虽然野生型轴突依赖于线粒体代谢，但在损伤后，在没有 Pten 和 Socs3 的情况下，能量产生由局部糖酵解支持。特异性抑制乳酸产生会阻碍损伤存活和再生的启动，而在上游减缓糖酵解会减缓再生启动、轴突伸长和能量产生。总的来说，这些观察结果表明，糖酵解 ATP 与持续的线粒体运输相结合，对于损伤诱导的轴突再生是必不可少的，为轴突再生的代谢基础提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98b6/11451009/d0d025de09be/JCB_202402133_Fig10.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98b6/11451009/d0d025de09be/JCB_202402133_Fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98b6/11451009/1b6a5ef097c0/JCB_202402133_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98b6/11451009/1ff2b024d9d1/JCB_202402133_FigS1.jpg
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A vesicular Warburg effect: Aerobic glycolysis occurs on axonal vesicles for local NAD+ recycling and transport.囊泡型瓦伯格效应：有氧糖酵解发生在轴突囊泡上，用于局部烟酰胺腺嘌呤二核苷酸（NAD+）的循环利用和运输。
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Aerobic glycolysis is the predominant means of glucose metabolism in neuronal somata, which protects against oxidative damage.
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有氧糖酵解是神经元胞体中葡萄糖代谢的主要方式，可防止氧化损伤。
Nat Neurosci. 2023 Dec;26(12):2081-2089. doi: 10.1038/s41593-023-01476-4. Epub 2023 Nov 23.
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Local glycolysis fuels actomyosin contraction during axonal retraction.局部糖酵解为轴突回缩过程中的肌球蛋白收缩供能。
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