| First Author | Guo Y | Year | 2015 |
| Journal | Lab Invest | Volume | 95 |
| Issue | 12 | Pages | 1439-49 |
| PubMed ID | 26524416 | Mgi Jnum | J:228083 |
| Mgi Id | MGI:5705191 | Doi | 10.1038/labinvest.2015.120 |
| Citation | Guo Y, et al. (2015) G-CSF promotes autophagy and reduces neural tissue damage after spinal cord injury in mice. Lab Invest 95(12):1439-49 |
| abstractText | 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-kappaB signal pathway in neurons after mechanical injury. We conclude that G-CSF promotes autophagy by inhibiting the NF-kappaB 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. |
