title: Time representation of mitochondrial morphology and function after acute spinal cord injury.
abstract: 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.
authors.affiliation: Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China.
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Jia
authors.affiliation: Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China.
authors.forename: Gang
authors.initials: G
authors.lastname: Li
authors.affiliation: Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China.
authors.forename: Zhen-Yu
authors.initials: ZY
authors.lastname: Zhang
authors.affiliation: Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China.
authors.forename: Hao-Tian
authors.initials: HT
authors.lastname: Li
authors.affiliation: Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China.
authors.forename: Ji-Quan
authors.initials: JQ
authors.lastname: Wang
authors.affiliation: Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China.
authors.forename: Zhong-Kai
authors.identifier: 0000-0002-6927-1787
authors.initials: ZK
authors.lastname: Fan
authors.affiliation: Department of Orthopedics, First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China.
authors.forename: Gang
authors.identifier: 0000-0001-6533-8764
authors.initials: G
authors.lastname: Lv
keywords: Caspase-3; NSFC; apoptosis; bioenergy; cytochrome c; fission; fusion; mitochondria; mitochondrial permeability; nerve regeneration; neural regeneration; oxidative damage; spinal cord injury