NDLI: Repulsive Wnt signaling inhibits axon regeneration following central nervous system injury

Content Provider	PubMed Central
Author	Liu, Yaobo Wang, Xiaofei Lu, Chin-chun Sherman, Rachel Steward, Oswald Xu, Xiao-ming Zou, Yimin
Abstract	Failure of axon regeneration in the mammalian central nervous system (CNS) is due in part to the presence of various inhibitory molecules, including myelin-associated proteins and proteoglycans enriched in glial scars. Here we evaluate whether axon guidance molecules also regulate regenerative growth after injury in adulthood. Wnts are a large family of axon guidance molecules, which can attract ascending axons and repel descending axons along the length of the developing spinal cord. Their expression (all 19 Wnts) is not detectable in normal adult spinal cord by in situ hybridization. However, three of them are clearly reinduced after spinal cord injury. Wnt1 and Wnt5a, encoding potent repellents of the descending corticospinal tract (CST) axons, were robustly and acutely induced broadly in the spinal cord gray matter following unilateral hemisection. Ryk, the conserved repulsive Wnt receptor, was also induced in the lesion area, and Ryk immunoreactivity was found on the lesioned CST axons. Wnt4, which attracts ascending sensory axons in development, was acutely induced in areas closer to the lesion than Wnt1 and Wnt5a. Injection of function-blocking Ryk antibodies into the dorsal bilateral hemisectioned spinal cord either prevented the retraction of CST axons or promoted their regrowth but clearly enhanced the sprouting of CST collateral branches around and beyond the injury site. Therefore, repulsive Wnt signaling may be a cause of cortical spinal tract axon retraction and inhibits axon sprouting following injury.
Related Links	http://dx.doi.org/10.1523/jneurosci.1939-08.2008
Ending Page	8382
Page Count	7
Starting Page	8376
File Format	PDF
ISSN	02706474
e-ISSN	15292401
Journal	The Journal of Neuroscience
Issue Number	33
Volume Number	28
Language	English
Publisher Date	2008-08-13
Access Restriction	Open
Subject Keyword	Neuroscience(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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