Journal
LABORATORY INVESTIGATION
Volume 95, Issue 12, Pages 1439-1449Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/labinvest.2015.120
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Funding
- National Natural Science Foundation of China [81100919]
- China postdoctoral science foundation [2014170647]
- postdoctoral science foundation of Shandong province [201203050]
- Scientific Research Foundation for Returned Scholars, Ministry of Education of China [21300005451001]
- Shangdong Province Young and Middle-Aged Scientists Research Awards Fund [BS2010YY041]
- Natural Science Foundation of Shandong Province [2012GSF11842, ZR2011HL070, ZR2015HM030]
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Granulocyte colony-stimulating factor (G-CSF) was investigated for its capacity to induce autophagy and related neuroprotective mechanisms in an acute spinal cord injury model. To accomplish this goal, we established a mouse spinal cord hemisection model to test the effects of recombinant human G-CSF. The results showed that autophagy was activated after spinal cord injury and G-CSF appears to induce a more rapid activation of autophagy within injured spinal cords as compared with that of non-treated animals. Apoptosis as induced in mechanically injured neurons with G-CSF treatment was enhanced after inhibiting autophagy by 3-methyladenine (3-MA), which partially blocked the neuroprotective effect of autophagy as induced by G-CSF. In addition, G-CSF inhibited the activity of the NF-kappa B signal pathway in neurons after mechanical injury. We conclude that G-CSF promotes autophagy by inhibiting the NF-kappa B signal pathway and protects neuronal structure after spinal cord injury. We therefore suggest that G-CSF, which rapidly induces autophagy after spinal cord injury to inhibit neuronal apoptosis, may thus provide an effective auxiliary therapeutic intervention for spinal cord injury.
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