Acute granulocyte macrophage-colony stimulating factor treatment modulates neuroinflammatory processes and promotes tactile recovery after spinal cord injury

Neuroscience ◽  
2017 ◽  
Vol 349 ◽  
pp. 144-164 ◽  
Author(s):  
Sandie Thomaty ◽  
Laurent Pezard ◽  
Christian Xerri ◽  
Jean-Michel Brezun
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Colony Stimulating Factor ◽  
Cord Injury ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Improvement in sensory function via granulocyte-macrophage colony-stimulating factor in rat spinal cord injury models

2013 ◽  
Vol 18 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Ji Yong Kim ◽  
Chang Hyun Oh ◽  
Xian Huang ◽  
Moon Hang Kim ◽  
Seung Hwan Yoon ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Colony Stimulating Factor ◽  
Rat Spinal Cord ◽  
Gm Csf ◽  
Cord Injury ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Object The aim in this study was to determine whether granulocyte-macrophage colony-stimulating factor (GM-CSF) leads to sensory improvement in rat spinal cord injury (SCI) models. Methods Thirty male Sprague-Dawley rats were included in this study: 10 in the sham group (laminectomy alone without SCI), 10 in the SCI group (SCI treated with phosphate-buffered saline), and 10 in the GM-CSF treatment group (SCI treated with GM-CSF). A locomotor function test and pain sensitivity test were conducted weekly for 9 weeks after SCI or sham injury. Spinal tissue samples from all rats were immunohistochemically examined for the expression of calcitonin gene-related peptide (CGRP) and abnormal sprouting at Week 9 post-SCI. Results Granulocyte-macrophage colony-stimulating factor treatment improves functional recovery after SCI. In the tactile withdrawal threshold and frequency of the hindlimb paw, the GM-CSF group always responded with a statistically significant lower threshold than the SCI group 9 weeks after SCI (p < 0.05). The response of the forelimb and hindlimb paws to cold in the GM-CSF group always reflected a statistically significant lower threshold than in the SCI group 9 weeks after injury (p < 0.05). Decreased CGRP expression, observed by density and distribution area, was noted in the GM-CSF group (optical density 113.5 ± 20.4) compared with the SCI group (optical density 143.1 ± 18.7; p < 0.05). Conclusions Treatment with GM-CSF results in functional recovery, improving tactile and cold sense recovery in a rat SCI model. Granulocyte-macrophage colony-stimulating factor also minimizes abnormal sprouting of sensory nerves after SCI.

Role of granulocyte—macrophage colony—stimulating factor in preventing apoptosis and improving functional outcome in experimental spinal cord contusion injury

2005 ◽  
Vol 2 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Yoon Ha ◽  
Young Soo Kim ◽  
Jin Mo Cho ◽  
Seung Hwan Yoon ◽  
So Ra Park ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuronal Death ◽  
Colony Stimulating Factor ◽  
Content Type ◽  
Gm Csf ◽  
N2a Cells ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Fine Print

Object. Granulocyte—macrophage colony—stimulating factor (GM-CSF) is a potent hemopoietic cytokine that stimulates stem cell proliferation in the bone marrow and inhibits apoptotic cell death in leukocytes. Its effects in the central nervous system, however, are still unclear. The present study was undertaken to determine if GM-CSF can rescue neuronal cells from apoptosis and improve neurological function in a spinal cord injury (SCI) model. Methods. To study the effect of GM-CSF on apoptotic neuronal death, the authors used a staurosporine-induced neuronal death model in an N2A cell line (in vitro) and in a rat SCI model (in vivo). The N2A cells were preincubated with GM-CSF for 60 minutes before being exposed to staurosporine for 24 hours. To inhibit GM-CSF, N2A cells were pretreated with antibodies against the GM-CSF receptor for 60 minutes. Clip compression was used to induce SCI. Animals were treated with daily doses of GM-CSF (20 µg/day) for 5 days. The number of apoptotic cells in the spinal cord and neurological improvements were assessed. Pretreatment with GM-CSF was found to protect N2A cells significantly from apoptosis, and neutralizing antibodies for the GM-CSF receptors inhibited the rescuing effect of GM-CSF on apoptosis. In the rat SCI model, neurological function improved significantly in the GM-CSF—treated group compared with controls treated with phosphate-buffered saline. Terminal deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick-end labeling staining showed that GM-CSF administration reduced apoptosis in the injured spinal cord. Conclusions. Treatment of SCI with GM-CSF showed beneficial effects. Neuronal protection against apoptosis is viewed as a likely mechanism underlying the therapeutic effect of GM-CSF in SCI.

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