| Background:After spinal cord injury,the clinical treatment cannot completely solve the problem with the body,because the glial scar,which could compromise the repair of injured neuron and axonal regeneration,forms in the spinal cord tissue.The Mitochondrial GTPase mitofusin-2(Mfn2)gene,also called the hyperplasia suppressor gene(HSG),and the Mfn2 has previously been reported to play a role in regulating cell proliferation,apoptosis and differentiation in a number of cell types.Objective: To analysis the expression tendency of Mfn2,and to discover the changes of GFAP’s expression during the glial scar formation induced by astrocytes’ activation in spinal cord injury.Then to explore whether reactive astrogliosis could be suppressed by Mfn2 overexpression.Methods: Allen’s weight-drop method was performed to prepare spinal cord injury models in rats expect the control group.SD rats were random allocated into control group,injury group,Adv-GFP group,Adv-Mfn2 group.Then each group was random allocated into 6h group,12 h group,24 h group,48 h group,testing the level of Mfn2,GFAP,PCNA,and GAP-43 expression.Results: The expression of GFAP protein was consistently increased after the spinal cord injury,and reached the peak at 24 h.The protein of PCNA also increased consistently and reached the peak at 12 h.Meanwhile,compared with control group,the expression of Mfn2 protein was down-regulated after the spinal cord injury,and reach the minimum at 12 h.Negative correlation exists between the expression of Mfn2 and GFAP.The expression of GAP-43 increased obviously at 24 h.After injecting the Adv-Mfn2,by contrasting groups at 24 h,the expression of Mfn2 was observably increased in Adv-Mfn2 group,while the GFAP and PCNA expression were markedly down-regulated.Conclusions: After spinal cord injury,the quiescent astrocytes changed into reactive mitotic cells,with proteins of GFAP markedly up-regulated,while the expression of Mfn2 protein was decreased.Overexpression of Mfn2 could inhibit reactive astrogliosis proliferation. |