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Updated: Aug 9, 2026
Synergetic Use of Neural Precursor Cells and Self-assembling Peptides in Experimental Cervical Spinal Cord Injury
Published on: February 23, 2015
Delayed GM-CSF treatment stimulates axonal regeneration and functional recovery in paraplegic rats via an increased
Delphine Bouhy1, Brigitte Malgrange, Sylvie Multon
1Research Center for Cellular and Molecular Neurobiology, University of Liège, Tour de Pathologie B36, 1étage, local 1/4A, CHU Sart-Tilman 4000 Liège, Belgium.
Abstract:
Macrophages (monocytes/microglia) could play a critical role in central nervous system repair. We have previously found a synchronism between the regression of spontaneous axonal regeneration and the deactivation of macrophages 3-4 wk after a compression-injury of rat spinal cord. To explore whether reactivation of endogenous macrophages might be beneficial for spinal cord repair, we have studied the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) in the same paraplegia model and in cell cultures. There was a significant, though transient, improvement of locomotor recovery after a single delayed intraperitoneal injection of 2 microg GM-CSF, which also increased significantly the expression of Cr3 and brain-derived neurotrophic factor (BDNF) by macrophages at the lesion site. At longer survival delays, axonal regeneration was significantly enhanced in GM-CSF-treated rats. In vitro, BV2 microglial cells expressed higher levels of BDNF in the presence of GM-CSF and neurons cocultured with microglial cells activated by GM-CSF generated more neurites, an effect blocked by a BDNF antibody. These experiments suggest that GM-CSF could be an interesting treatment option for spinal cord injury and that its beneficial effects might be mediated by BDNF.
Insights
Granulocyte-macrophage colony stimulating factor (GM-CSF) improved locomotor recovery and axonal regeneration in spinal cord injury models. This suggests GM-CSF may be a viable treatment option, potentially mediated by brain-derived neurotrophic factor (BDNF).
Area of Science:
- Neuroscience
- Immunology
- Regenerative Medicine
Background:
- Macrophages are crucial for central nervous system repair.
- Macrophage deactivation correlates with reduced axonal regeneration after spinal cord injury.
- Investigating macrophage reactivation for therapeutic benefit is warranted.
Purpose of the Study:
- To determine if granulocyte-macrophage colony stimulating factor (GM-CSF) can reactivate endogenous macrophages and promote spinal cord repair.
- To assess the effects of GM-CSF on locomotor recovery, axonal regeneration, and macrophage activity in a rat spinal cord injury model.
- To investigate the in vitro effects of GM-CSF on microglial cells and neuronal growth.
Main Methods:
- A rat spinal cord compression-injury model was used.
- Granulocyte-macrophage colony stimulating factor (GM-CSF) was administered intraperitoneally.
- Locomotor recovery, axonal regeneration, macrophage marker expression (Cr3), and brain-derived neurotrophic factor (BDNF) levels were assessed.
- In vitro studies involved BV2 microglial cells and neuronal co-cultures.
Main Results:
- A single delayed GM-CSF injection led to transient improvement in locomotor recovery.
- GM-CSF significantly increased Cr3 and BDNF expression by macrophages at the lesion site.
- Axonal regeneration was significantly enhanced in GM-CSF treated rats at longer survival times.
- In vitro, GM-CSF increased BDNF in microglial cells and promoted neurite outgrowth in co-cultures, an effect blocked by a BDNF antibody.
Conclusions:
- GM-CSF shows potential as a treatment for spinal cord injury.
- The beneficial effects of GM-CSF may be mediated by increased BDNF production.
- Reactivating macrophages with GM-CSF could be a promising strategy for enhancing spinal cord repair.
