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

作     者：Zhi-qiang Jia Gang Li Zhen-yu Zhang Hao-tian Li Ji-quan Wang Zhong-kai Fan Gang Lv 

作者机构：Department of Orthopedics First Affiliated Hospital of Liaoning Medical University 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2016年第11卷第1期

页      面：137-143页

核心收录：

学科分类：1002[医学-临床医学] 100210[医学-外科学(含：普外、骨外、泌尿外、胸心外、神外、整形、烧伤、野战外)] 10[医学] 

基　　金：supported by the National Natural Science Foundation of China,No.81272074 the Scientific Research Foundation Project for Doctors in Liaoning Province of China,No.20121094 Aohongboze Graduate Sci-tech Innovation Foundation the President Fund of Liaoning Medical University of China,No.2013003 

主　　题：nerve regeneration spinal cord injury mitochondria fusion fission oxidative damage bioenergy mitochondrial permeability cytochrome c Caspase 3 apoptosis NSFC neural regeneration 

摘      要：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.