3月4,日本名古屋大學(xué)研究生院教授松本邦弘和同事在英國(guó)期刊《自然—神經(jīng)學(xué)》(Nature Neuroscience)網(wǎng)絡(luò)版上報(bào)告說,,他們研究了線蟲體內(nèi)約1.5萬(wàn)個(gè)蛋白質(zhì),,發(fā)現(xiàn)在神經(jīng)細(xì)胞外部誘導(dǎo)這種細(xì)胞增殖的分泌蛋白和位于神經(jīng)細(xì)胞膜內(nèi)的受體蛋白,在軸突再生方面發(fā)揮著重要作用。這兩種蛋白質(zhì)的結(jié)合,可幫助軸突再生,。
線蟲的神經(jīng)細(xì)胞凸起物——神經(jīng)軸突在意外斷裂后,會(huì)有少數(shù)軸突神奇地復(fù)合再生,。它們是如何做到的呢,?日本研究者發(fā)現(xiàn),,這種“再續(xù)前緣”得益于兩種蛋白質(zhì)的特殊作用,。
神經(jīng)軸突是神經(jīng)細(xì)胞的輸出通道,負(fù)責(zé)將該細(xì)胞發(fā)出的神經(jīng)沖動(dòng)傳遞給其他神經(jīng)細(xì)胞或肌肉,、腺體,。如果軸突徹底斷裂,神經(jīng)就無(wú)法再發(fā)揮作用,。
在實(shí)驗(yàn)中,,研究人員通過基因操作,使線蟲能大量合成這兩種蛋白質(zhì),,然后切斷它們的神經(jīng)軸突,。最后,在斷開的軸突中有40%至60%的軸突能夠再生,。而在正常情況下,,線蟲的軸突被切斷后只有5%能再生。
松本邦弘認(rèn)為,,某些人體蛋白質(zhì)的功能可能與上述兩種線蟲蛋白質(zhì)類似,,如能在今后的研究中確認(rèn)這些人體蛋白質(zhì)的“促進(jìn)再生”功效,并把它們注射到神經(jīng)受損者的特定部位,,就有可能使嚴(yán)重受傷的神經(jīng)復(fù)合再生,。(生物谷Bioon.com)
doi:10.1038/nn.3052
PMC:
PMID:
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.