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Time representation of mitochondrial morphology and function after acute spinal cord injury.

Authors: Jia, Zhi-Qiang  Li, Gang  Zhang, Zhen-Yu  Li, Hao-Tian  Wang, Ji-Quan  Fan, Zhong-Kai  Lv, Gang 
Citation: Jia ZQ, etal., Neural Regen Res. 2016 Jan;11(1):137-43. doi: 10.4103/1673-5374.175061.
Pubmed: (View Article at PubMed) PMID:26981103
DOI: Full-text: DOI:10.4103/1673-5374.175061

Changes in mitochondrial morphology and function play an important role in secondary damage after acute spinal cord injury. We recorded the time representation of mitochondrial morphology and function in rats with acute spinal cord injury. Results showed that mitochondria had an irregular shape, and increased in size. Mitochondrial cristae were disordered and mitochondrial membrane rupture was visible at 2-24 hours after injury. Fusion protein mitofusin 1 expression gradually increased, peaked at 8 hours after injury, and then decreased to its lowest level at 24 hours. Expression of dynamin-related protein 1, amitochondrial fission protein, showed the opposite kinetics. At 2-24 hours after acute spinal cord injury, malondialdehyde content, cytochrome c levels and caspase-3 expression were increased, but glutathione content, adenosine triphosphate content, Na(+)-K(+)-ATPase activity and mitochondrial membrane potential were gradually reduced. Furthermore, mitochondrial morphology altered during the acute stage of spinal cord injury. Fusion was important within the first 8 hours, but fission played a key role at 24 hours. Oxidative stress was inhibited, biological productivity was diminished, and mitochondrial membrane potential and permeability were reduced in the acute stage of injury. In summary, mitochondrial apoptosis is activated when the time of spinal cord injury is prolonged.


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RGD Object Information
RGD ID: 12910837
Created: 2017-06-26
Species: All species
Last Modified: 2017-06-26
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.