کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6263800 1613917 2013 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research ReportMitochondrial fusion and fission after spinal sacord injury in rats
ترجمه فارسی عنوان
گزارش تحقیقاتی همجوشی متقاطع و شکافت پس از آسیب نخاعی صرع در موش صحرایی
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی


- We investigated change of mitochondrial morphology in neurons with the impact of SCI.
- Protein expression and mRNA of mitochondrial fission and fusion proteins were analyzed with the impact of SCI.
- The mechanisms whereby the dynamics and function of mitochondria regulate neuron cell injury during SCI were discussed.

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1522, 19 July 2013, Pages 59-66
نویسندگان
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