标题：Granulocyte colony-stimulating factor improves neuron survival in experimental spinal cord injury by regulating nucleophosmin-1 expression
作者机构：[Guo, Y] Key Laboratory of the Ministry of Education for Experimental Teratology, Department of Histology and Embryology, Shandong University School o 更多
通讯作者地址：[Hao, AJ]Shandong Univ, Sch Med, Dept Histol & Embryol, 44 Wenhua Xi Rd, Jinan 250012, Shandong, Peoples R China.
来源：Journal of Neuroscience Research
关键词：Apoptosis;Granulocyte colony-stimulating factor;Nucleophosmin 1;P53;Spinal cord injury
摘要：Granulocyte colony-stimulating factor (G-CSF) and its related mechanisms were investigated to assess the potential for this factor to exert neuroprotective effects against spinal cord injury in mice. Recombinant human granulocyte colony-stimulating factor (rhG-CSF) was injected into mice spinal cord hemisection models. Locomotor activity was assessed by using the Basso-Bettie-Bresnahan scale. Neurons isolated from spinal cords were cultured in vitro and used in a neuronal mechanical injury model. Three treatment groups were compared with this model, 1) G-CSF, 2) G-CSF+NSC348884 (a nucleophosmin 1-specific inhibitor), and 3) NSC348884. Immunofluorescence staining and Western blotting were performed to analyze the expression of G-CSF and nucleophosmin 1 (Npm1). TUNEL staining was performed to analyze apoptosis after G-CSF treatment. We found that the G-CSF receptor (G-CSFR) and Npm1 were expressed in neurons and that Npm1 expression was induced after G-CSF treatment. G-CSF inhibited neuronal apoptosis. NSC348884 induced p53-dependent cell apoptosis and partially blocked the neuroprotective activity of G-CSF on neurons in vitro. G-CSF promoted locomotor recovery and demonstrated neuroprotective effects in an acute spinal cord injury model. The mechanism of G-CSF\'s neuroprotection may be related in part to attenuating neuronal apoptosis by NPM1.