Journal
JOURNAL OF NEUROSCIENCE
Volume 28, Issue 38, Pages 9363-9376Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1447-08.2008
Keywords
nervous system; macrophages; neurotrophins; sciatic nerve; spinal cord injury; angiogenesis
Categories
Funding
- Natural Sciences and Engineering Research Council of Canada
- Rx& D Health Research Foundation
- Canadian Institutes of Health Research (CIHR)
- CIHR Doctoral Research Award
Ask authors/readers for more resources
The role of CD11b(+) myeloid cells in axonal regeneration was assessed using axonal injury models and CD11b-TKmt-30 mice expressing a mutated HSV-1 thymidine kinase (TK) gene regulated by the myeloid-specific CD11b promoter. Continuous delivery of ganciclovir at a sciatic nerve lesion site greatly decreased the number of granulocytes/inflammatory monocytes and macrophages in the distal stump of CD11b-TKmt-30 mice. Axonal regeneration and locomotor function recovery were severely compromised in ganciclovir-treated CD11b-TKmt-30 mice. This was caused by an unsuitable growth environment rather than an altered regeneration capacity of neurons. In absence of CD11b(+) cells, the clearance of inhibitory myelin debris was prevented, neurotrophin synthesis was abolished, and blood vessel formation/ maintenance was severely compromised in the sciatic nerve distal stump. Spinal cord-injured axons also failed to regenerate through peripheral nerve grafts in the absence of CD11b(+) cells. Therefore, myeloid cells support axonal regeneration and functional recovery by creating a growth-permissive milieu for injured axons.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available