PI3K-GSK3 signalling regulates mammalian axon regeneration by inducing the expression of Smad1

Authors
SaijilafuHur, Eun-MiLiu, Chang-MeiJiao, ZhongxianXu, Wen-LinZhou, Feng-Quan
Issue Date
2013-10
Publisher
NATURE PUBLISHING GROUP
Citation
NATURE COMMUNICATIONS, v.4
Abstract
In contrast to neurons in the central nervous system, mature neurons in the mammalian peripheral nervous system (PNS) can regenerate axons after injury, in part, by enhancing intrinsic growth competence. However, the signalling pathways that enhance the growth potential and induce spontaneous axon regeneration remain poorly understood. Here we reveal that phosphatidylinositol 3-kinase (PI3K) signalling is activated in response to peripheral axotomy and that PI3K pathway is required for sensory axon regeneration. Moreover, we show that glycogen synthase kinase 3 (GSK3), rather than mammalian target of rapamycin, mediates PI3K-dependent augmentation of the growth potential in the PNS. Furthermore, we show that PI3K-GSK3 signal is conveyed by the induction of a transcription factor Smad1 and that acute depletion of Smad1 in adult mice prevents axon regeneration in vivo. Together, these results suggest PI3K-GSK3-Smad1 signalling as a central module for promoting sensory axon regeneration in the mammalian nervous system.
Keywords
DORSAL-ROOT GANGLION; C-JUN; CONDITIONING LESION; GROWTH CONE; GENETIC DISSECTION; SCHWANN-CELLS; SPINAL-CORD; ACTIVATION; NERVE; AXOTOMY; DORSAL-ROOT GANGLION; C-JUN; CONDITIONING LESION; GROWTH CONE; GENETIC DISSECTION; SCHWANN-CELLS; SPINAL-CORD; ACTIVATION; NERVE; AXOTOMY; Biological sciences; Cell biology; Neuroscience
ISSN
2041-1723
URI
https://pubs.kist.re.kr/handle/201004/127587
DOI
10.1038/ncomms3690
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KIST Article > 2013
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