title: Identification of mitochondria translation elongation factor Tu as a contributor to oxidative damage of postburn myocardium.
abstract: Mitochondrial damage plays an important role in mediating postburn cardiac injury. To elucidate the pivotal mitochondrial proteins and pathways underlying postburn cardiac injury, mitochondria were purified from control and postburn rat hearts. 2-dimensional gel electrophoresis (2-DE) and HPLC-chip-MS/MS analyses revealed 9 differentially expressed proteins, 3 of which were further validated by Western blotting. The differential expression of these mitochondrial proteins was accompanied by increased levels of oxidative cardiac damage and decreased levels of cardiac output. One of the differentially expressed proteins, mitochondria translation elongation factor Tu (EF-Tumt), was hypothesized to contribute crucially to postburn oxidative cardiac damage. The small interfering RNA (siRNA)-mediated downregulation of EF-Tumt in cultured rat cardiomyocytes increased reactive oxygen species (ROS) generation and protein carbonyl levels, and led to cell damage. The potential pathway of this process was associated with respiratory chain complex I deficiency. Together, these results demonstrate the mitochondrial responses to severe burn, and indicate a pathway by which decreased EF-Tumt expression mediates oxidative damage in postburn myocardium.
authors.affiliation: Institute of Burn Research, Southwest Hospital, Third Military Medical University, State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing, 400038, PR China.
authors.forename: Dong-xia
authors.initials: DX
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Yan
authors.forename: Jiong-yu
authors.initials: JY
authors.lastname: Hu
authors.forename: Jia-ping
authors.initials: JP
authors.lastname: Zhang
authors.forename: Miao
authors.initials: M
authors.lastname: Teng
authors.forename: Da-li
authors.initials: DL
authors.lastname: Tong
authors.forename: Fei
authors.initials: F
authors.lastname: Xiang
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhang
authors.forename: Ya-dong
authors.initials: YD
authors.lastname: Fang
authors.forename: Guang-ping
authors.initials: GP
authors.lastname: Liang
authors.forename: Yue-sheng
authors.initials: YS
authors.lastname: Huang
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism* / Q000473:pathology; D042967:Electron Transport Complex I / Q000378:metabolism; D005786:Gene Expression Regulation; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000473:pathology; D024101:Mitochondrial Proteins / Q000378:metabolism*; D009124:Muscle Proteins / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D010444:Peptide Elongation Factor Tu / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D024101:Mitochondrial Proteins; D009124:Muscle Proteins; D017382:Reactive Oxygen Species; D010444:Peptide Elongation Factor Tu; D042967:Electron Transport Complex I