Mitochondrial fusion and fission after spinal sacord injury in rats
Mitochondrial fusion and fission after spinal sacord injury in rats
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DOI：
10.1016/j.brainres.2013.05.033
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发表时间：
2013-07-19
期刊：
影响因子：
2.9
通讯作者：
Guo, Zhan-Peng
中科院分区：
文献类型：
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作者：
Cao, Yang;Lv, Gang;Guo, Zhan-Peng
线粒体负责协调细胞能量的产生，是维持生命的核心，也是细胞死亡的守门人。它的形态是动态的，受连续和平衡的裂变和聚变事件的控制。本研究通过对大鼠脊髓损伤后线粒体动力学和功能的分析，进一步探讨线粒体调控脊髓损伤细胞的机制。利用成年大鼠脊髓损伤模型，我们发现在脊髓损伤后3 h和6 h，脊髓损伤组大鼠神经元中每区域线粒体的绝对数量明显少于假手术组，个体线粒体横截面积明显大于假手术组，在脊髓损伤后12 h和24 h则相反。Western blot和RT-PCR检测结果显示，脊髓损伤后3 h和6 h，线粒体融合相关基因（Mfn1和Mfn2）蛋白和mRNA水平下降，分裂相关基因（Drp1和Fis1）蛋白和mRNA水平升高。在脊髓损伤后12 h和24 h， Mfn1、Mfn2、Drp1和Fis1的表达方向相反。综上所述，本研究结果显示，我们的大鼠脊髓损伤模型在脊髓损伤后3 h和6 h线粒体有伸长和融合的趋势，在脊髓损伤后12 h和24 h线粒体有分裂的趋势。这些发现对我们理解脊髓损伤后线粒体动力学和功能的机制具有重要意义。线粒体融合可能是脊髓损伤后6小时内改善脊髓功能的潜在靶点。线粒体融合可能在脊髓损伤后12-24小时受到抑制，以改善脊髓损伤后的功能预后。爱思唯尔B.V.版权所有
Responsible for orchestrating cellular energy production, mitochondria are central to the maintenance of life and the gatekeepers of cell death. Its morphology is dynamic and controlled by continual and balanced fission and fusion events. In this study, we analyzed the mitochondrial dynamics and functions after spinal cord injury in rats and further to discuss the mechanisms of the mitochondria regulated cell injury during SCI. Using adult rat spinal cord injury model, it was found that the absolute number of mitochondria per area was significantly less and the individual mitochondrial cross-sectional area was significantly greater in the neurons of rats in SCI group than in the sham-operated group at 3 h and 6 h after SCI, and the reverse pattern at 12 h and 24 h after SCI. The results from Western blot and RT-PCR assays showed that the protein and mRNA levels of mitochondrial fusion-related genes (Mfn1 and Mfn2) decreased and fission-related genes (Drp1 and Fis1) increased at 3 h and 6 h after SCI. At 12 h and 24 h after SCI the reverse pattern of Mfn1, Mfn2, Drp1 and Fis1 expression was found. Taken together the results of the present study showed the mitochondrial tendency of elongation and fusion in the injured spinal cord at 3 h and 6 h after SCI, and the tendency of mitochondrial fission at 12 h and 24 h after SCI in our SCI models of rat. These findings have important implications for our understanding of the mechanisms of mitochondrial dynamics and functions after SCI injury. And mitochondrial fusion may potentially be used as a target for improving spinal cord function in the first 6 h after SCI. Mitochondrial fusion may be inhibited at 12-24 h after SCI for improving functional outcomes following SCI. Crown Copyright (c) 2013 Published by Elsevier B.V. All rights reserved.