title: Acute high-altitude hypoxic brain injury: Identification of ten differential proteins.
abstract: Hypobaric hypoxia can cause severe brain damage and mitochondrial dysfunction, and is involved in hypoxic brain injury. However, little is currently known about the mechanisms responsible for mitochondrial dysfunction in hypobaric hypoxic brain damage. In this study, a rat model of hypobaric hypoxic brain injury was established to investigate the molecular mechanisms associated with mitochondrial dysfunction. As revealed by two-dimensional electrophoresis analysis, 16, 21, and 36 differential protein spots in cerebral mitochondria were observed at 6, 12, and 24 hours post-hypobaric hypoxia, respectively. Furthermore, ten protein spots selected from each hypobaric hypoxia subgroup were similarly regulated and were identified by mass spectrometry. These detected proteins included dihydropyrimidinase-related protein 2, creatine kinase B-type, isovaleryl-CoA dehydrogenase, elongation factor Ts, ATP synthase beta-subunit, 3-mercaptopyruvate sulfurtransferase, electron transfer flavoprotein alpha-subunit, Chain A of 2-enoyl-CoA hydratase, NADH dehydrogenase iron-sulfur protein 8 and tropomyosin beta chain. These ten proteins are all involved in the electron transport chain and the function of ATP synthase. Our findings indicate that hypobaric hypoxia can induce the differential expression of several cerebral mitochondrial proteins, which are involved in the regulation of mitochondrial energy production.
authors.affiliation: Department of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
authors.forename: Jianyu
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
authors.forename: Yuting
authors.initials: Y
authors.lastname: Qi
authors.affiliation: Department of Hepatobiliary, Tianjin Third Central Hospital, Tianjin 300170, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China ; Tianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Cui
authors.affiliation: Tianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
authors.forename: Haiying
authors.initials: H
authors.lastname: Gong
authors.affiliation: Department of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
authors.forename: Yaxiao
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China ; Tianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
authors.forename: Lingzhi
authors.initials: L
authors.lastname: Li
authors.affiliation: Tianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
authors.forename: Yongliang
authors.initials: Y
authors.lastname: Zhang
keywords: brain injury; cerebral edema; cognitive function; differential expression; electron transport chain; energy metabolism; grants-supported paper; hypobaric hypoxia; mitochondria; neural regeneration; neuroregeneration; proteomics