神经损伤之后的远距离、大范围修复已在周围神经系统中得到演示，但这种强有力的再生在中枢神经系统中却很罕见。以前的研究工作观察到了在对再生信号作用通道进行分子操纵之后的一些修复，但这些修复作用经常会在两星期后逐渐减小。
Zhigang He及其同事识别出了对信号作用通道的一种修饰，它能在一次神经挤压损伤后促进增强的外显子再生。这些被操纵的通道协同作用，来促进与生长相关的基因的表达，这些基因能够保持足够高的水平，以维持远距离的再生生长。（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.
