title: G-CSF promotes autophagy and reduces neural tissue damage after spinal cord injury in mice.
abstract: 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-κB signal pathway in neurons after mechanical injury. We conclude that G-CSF promotes autophagy by inhibiting the NF-κB 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.
authors.affiliation: Key Laboratory of the Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School of Medicine, Jinan, China.
authors.forename: Yuji
authors.initials: Y
authors.lastname: Guo
authors.affiliation: Key Laboratory of the Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School of Medicine, Jinan, China.
authors.forename: Shangming
authors.initials: S
authors.lastname: Liu
authors.affiliation: Key Laboratory of the Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School of Medicine, Jinan, China.
authors.forename: Xianghong
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Key Laboratory of the Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School of Medicine, Jinan, China.
authors.forename: Liyan
authors.initials: L
authors.lastname: Wang
authors.affiliation: Institute of Developmental Biology, College of Life Science, Shandong University, Jinan, China.
authors.forename: Jiangang
authors.initials: J
authors.lastname: Gao
authors.affiliation: Department of Obstetrics, Maternal and Children Health Hospital of Jinan City, Jinan, China.
authors.forename: Aiqing
authors.initials: A
authors.lastname: Han
authors.affiliation: Key Laboratory of the Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School of Medicine, Jinan, China.
authors.forename: Aijun
authors.initials: A
authors.lastname: Hao
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives; D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D002478:Cells, Cultured; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000378:metabolism*; D006801:Humans; D008124:Locomotion; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D009474:Neurons / Q000502:physiology; D011897:Random Allocation; D011994:Recombinant Proteins; D020127:Recovery of Function; D013119:Spinal Cord Injuries / Q000378:metabolism*
chemical_list: D016328:NF-kappa B; D011994:Recombinant Proteins; D016179:Granulocyte Colony-Stimulating Factor; C025946:3-methyladenine; D000225:Adenine