小柯机器人

少突胶质细胞通过分泌铁蛋白重链为神经元提供抗氧化防御功能，这一成果由德国慕尼黑工业大学Mikael Simons和德国神经退行性疾病中心（DZNE）Anja Schneider研究组合作取得。相关论文在线发表在2020年6月11日的《细胞-代谢》杂志上。

为了鉴定神经胶质细胞产生的对神经元具有重要功能的分子，研究人员利用果蝇作为工具进行了筛选，随后将发现的结果在小鼠中进行了验证。研究发现在神经胶质分泌途径中，发挥功能的货物受体通过调节铁平衡来维持轴突的完整性。研究人员发现铁蛋白重链是关键的分泌物，这是保护铁介导的铁蛋白轴突损伤所必需的。

在小鼠中，少突胶质细胞高度表达铁蛋白重链，并通过涉及细胞外囊泡的非常规分泌途径分泌。破坏少突胶质细胞中细胞外小泡的释放或铁蛋白重链的表达会引起小鼠神经元丢失和氧化损伤。这些数据揭示了少突胶质细胞在抗氧化防御系统和神经元抵抗铁介导细胞毒性中的作用。

据了解，在进化上，胶质细胞的保守功能维持了神经元的代谢和结构。

附：英文原文

Title: Oligodendrocytes Provide Antioxidant Defense Function for Neurons by Secreting Ferritin Heavy Chain

Author: Chaitali Mukherjee, Tina Kling, Belisa Russo, Kerstin Miebach, Eva Kess, Martina Schifferer, Liliana D. Pedro, Ulrich Weikert, Maryam K. Fard, Nirmal Kannaiyan, Moritz Rossner, Marie-Louise Aicher, Sandra Goebbels, Klaus-Armin Nave, Eva-Maria Krmer-Albers, Anja Schneider, Mikael Simons

Issue&Volume: 2020-06-11

Abstract: An evolutionarily conserved function of glia is to provide metabolic and structuralsupport for neurons. To identify molecules generated by glia and with vital functionsfor neurons, we used Drosophila melanogaster as a screening tool, and subsequently translated the findings to mice. We found thata cargo receptor operating in the secretory pathway of glia was essential to maintainaxonal integrity by regulating iron buffering. Ferritin heavy chain was identifiedas the critical secretory cargo, required for the protection against iron-mediatedferroptotic axonal damage. In mice, ferritin heavy chain is highly expressed by oligodendrocytesand secreted by employing an unconventional secretion pathway involving extracellularvesicles. Disrupting the release of extracellular vesicles or the expression of ferritinheavy chain in oligodendrocytes causes neuronal loss and oxidative damage in mice.Our data point to a role of oligodendrocytes in providing an antioxidant defense systemto support neurons against iron-mediated cytotoxicity.

DOI: 10.1016/j.cmet.2020.05.019

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30300-4

Cell Metabolism：《细胞—代谢》，创刊于2005年。隶属于细胞出版社，最新IF：31.373
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