神經(jīng)損傷之后的遠(yuǎn)距離、大范圍修復(fù)已在周?chē)窠?jīng)系統(tǒng)中得到演示,，但這種強(qiáng)有力的再生在中樞神經(jīng)系統(tǒng)中卻很罕見(jiàn),。以前的研究工作觀察到了在對(duì)再生信號(hào)作用通道進(jìn)行分子操縱之后的一些修復(fù)，但這些修復(fù)作用經(jīng)常會(huì)在兩星期后逐漸減小,。
Zhigang He及其同事識(shí)別出了對(duì)信號(hào)作用通道的一種修飾,，它能在一次神經(jīng)擠壓損傷后促進(jìn)增強(qiáng)的外顯子再生。這些被操縱的通道協(xié)同作用,，來(lái)促進(jìn)與生長(zhǎng)相關(guān)的基因的表達(dá),，這些基因能夠保持足夠高的水平,，以維持遠(yuǎn)距離的再生生長(zhǎng)。（生物谷Bioon.com）
doi:10.1038/nature10594
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Sustained axon regeneration induced by co-deletion of PTEN and SOCS3
Fang Sun, Kevin K. Park, Stephane Belin, Dongqing Wang, Tao Lu, Gang Chen, Kang Zhang, Cecil Yeung, Guoping Feng, Bruce A. Yankner & Zhigang He
A formidable challenge in neural repair in the adult central nervous system (CNS) is the long distances that regenerating axons often need to travel in order to reconnect with their targets. Thus, a sustained capacity for axon regeneration is critical for achieving functional restoration. Although deletion of either phosphatase and tensin homologue (PTEN), a negative regulator of mammalian target of rapamycin (mTOR), or suppressor of cytokine signalling 3 (SOCS3), a negative regulator of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, in adult retinal ganglion cells (RGCs) individually promoted significant optic nerve regeneration, such regrowth tapered off around 2?weeks after the crush injury1, 2. Here we show that, remarkably, simultaneous deletion of both PTEN and SOCS3 enables robust and sustained axon regeneration. We further show that PTEN and SOCS3 regulate two independent pathways that act synergistically to promote enhanced axon regeneration. Gene expression analyses suggest that double deletion not only results in the induction of many growth-related genes, but also allows RGCs to maintain the expression of a repertoire of genes at the physiological level after injury. Our results reveal concurrent activation of mTOR and STAT3 pathways as key for sustaining long-distance axon regeneration in adult CNS, a crucial step towards functional recovery.
