脊髓损伤后自噬在轴突变性中作用.docVIP

脊髓损伤后自噬在轴突变性中的作用 大自噬是一种体内平衡机制，负责降解零散细胞质、长寿蛋白和整个细胞器，其特征是称为自噬体的双膜泡形成。先前已经有证据表明，健康的新生轴突自噬体形式和吞噬产物在轴突末端优先形成。几项研究显示出轴突变性可诱导自噬，但缺乏脊髓损伤后轴突自噬相关蛋白的精确表征。 在发表于《中国神经再生研究（英文版）》杂志2015年2月第2期的文章中，德国哥廷根医科大学Paul Lingor教授和其同事讨论了他们实验室的最新研究：关于脊髓损伤后轴突退化中与时间相关的调控自噬神经特点。他们发现，ULK1和Atg5这两个自噬蛋白质在诱导自噬过程中位于自噬体形成部位，而脊髓损伤后则积聚在轴索回缩球内。关键自噬蛋白质ATG7在损伤后早期会有上调。与ULK1和Atg5不同，ATG7蛋白质弥散在整个轴突区域。最后，损伤后30分钟，轴突LC3阳性自噬体的数量开始增加，但令人惊讶的是即使在损伤后6个星期，其仍保持在较高水平。因此，这些结果表明脊髓损伤后关键自噬角色在轴突退化早期持续增加，这可能会在该疾病过程中促进轴突变性。轴索回缩球内的ULK1和Atg5积累表明轴索回缩球位置不变，此处轴突损伤后会发生自噬体生物合成。他们也在其他模型系统中观察了类似的轴突变性过程。因此，自噬相关蛋白干扰可能是创伤性、退行性中枢神经系统疾病和轴突变性有前途的治疗靶点。 Article: Autophagy in degenerating axons following spinal cord injury: evidence for autophagosome biogenesis in retraction bulbs by Vinicius T. Ribas1, Paul Lingor1,2 (1 Department of Neurology, University Medicine G?ttingen, 37075 G?ttingen, Germany; 2 Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), G?ttingen, Germany) Ribas VT, Lingor P (2015) Autophagy in degenerating axons following spinal cord injury: evidence for autophagosome biogenesis in retraction bulbs. Neural Regen Res 10(2):198-200. 欲获更多资讯： Neural Regen Res Autophagy in degenerating axons following spinal cord injury Macroautophagy is a homeostatic mechanism responsible for the degradation of bulk cytoplasm, long-lived proteins, and entire organelles and is characterized by the formation of double-membrane vesicles called autophagosomes. It has been previously shown that in healthy axons nascent autophagosomes form and engulf cargo preferentially at the axonal tip. Several studies showed an induction of autophagy in axonal degeneration, but the precise characterization of autophagy-related proteins in the axons after spinal cord injury (SCI) was lacking. Here, Neural Regeneration Research (Vol. 10, No. 2, 2015), Prof. Paul Lingor (University Medicine G?ttingen, Germany) and his coworker discuss a recent study in which they characterized the time-dependent regulation autophagy in degenerating axons after