3月4，日本名古屋大学研究生院教授松本邦弘和同事在英国期刊《自然—神经学》（Nature Neuroscience）网络版上报告说，他们研究了线虫体内约1.5万个蛋白质，发现在神经细胞外部诱导这种细胞增殖的分泌蛋白和位于神经细胞膜内的受体蛋白，在轴突再生方面发挥着重要作用。这两种蛋白质的结合，可帮助轴突再生。
线虫的神经细胞凸起物——神经轴突在意外断裂后，会有少数轴突神奇地复合再生。它们是如何做到的呢？日本研究者发现，这种“再续前缘”得益于两种蛋白质的特殊作用。
神经轴突是神经细胞的输出通道，负责将该细胞发出的神经冲动传递给其他神经细胞或肌肉、腺体。如果轴突彻底断裂，神经就无法再发挥作用。
在实验中，研究人员通过基因操作，使线虫能大量合成这两种蛋白质，然后切断它们的神经轴突。最后，在断开的轴突中有40%至60%的轴突能够再生。而在正常情况下，线虫的轴突被切断后只有5%能再生。
松本邦弘认为，某些人体蛋白质的功能可能与上述两种线虫蛋白质类似，如能在今后的研究中确认这些人体蛋白质的“促进再生”功效，并把它们注射到神经受损者的特定部位，就有可能使严重受伤的神经复合再生。（生物谷Bioon.com）
doi:10.1038/nn.3052
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The growth factor SVH-1 regulates axon regeneration in C. elegans via the JNK MAPK cascade
Chun Li; Naoki Hisamoto; Paola Nix; Shuka Kanao; Tomoaki Mizuno; Michael Bastiani; Kunihiro Matsumoto
The ability of neurons to undergo regenerative growth after injury is governed by cell-intrinsic and cell-extrinsic regeneration pathways. These pathways represent potential targets for therapies to enhance regeneration. However, the signaling pathways that orchestrate axon regeneration are not well understood. In Caenorhabditis elegans, the Jun N-terminal kinase (JNK) and p38 MAP kinase (MAPK) pathways are important for axon regeneration. We found that the C. elegans SVH-1 growth factor and its receptor, SVH-2 tyrosine kinase, regulate axon regeneration. Loss of SVH-1–SVH-2 signaling resulted in a substantial defect in the ability of neurons to regenerate, whereas its activation improved regeneration. Furthermore, SVH-1–SVH-2 signaling was initiated extrinsically by a pair of sensory neurons and functioned upstream of the JNK-MAPK pathway. Thus, SVH-1–SVH-2 signaling via activation of the MAPK pathway acts to coordinate neuron regeneration response after axon injury.
