title: Heat shock protein expression and change of cytochrome c oxidase activity: presence of two phylogenic old systems to protect tissues in ischemia and reperfusion.
abstract: Induction of heat shock proteins (hsp) has been shown to protect cells from ischemia by providing transient tolerance against myocardial injury and improving postischemic functional recovery. Attenuation of ATP depletion and earlier restoration of ATP content on reperfusion are thought to play a role in this scenario. Hsp induction is accompanied by altered enzyme activity of the respiratory chain, the major generator of ATP under physiological conditions. This report addresses the question whether processing and final assembly of the active holoenzyme cytochrome c oxidase (CcO, complex IV), member of the respiratory chain, is compromised under hypoxic conditions unless protected by stress proteins. Special focus is laid on function of the enzyme's subunits and importance of cellular energy availability and maintenance.
authors.affiliation: Biomedical Research Center, Philipps-University Marburg, Marburg, Germany. vogts@med.uni-marburg.de
authors.forename: Sebastian
authors.initials: S
authors.lastname: Vogt
authors.forename: Irene
authors.initials: I
authors.lastname: Portig
authors.forename: Mark
authors.initials: M
authors.lastname: Irqsusi
authors.forename: Volker
authors.initials: V
authors.lastname: Ruppert
authors.forename: Petra
authors.initials: P
authors.lastname: Weber
authors.forename: Rabia
authors.initials: R
authors.lastname: Ramzan
mesh_terms: D000818:Animals; D003576:Electron Transport Complex IV / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000378:metabolism; D006801:Humans; D009203:Myocardial Infarction / Q000378:metabolism*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control
chemical_list: D006360:Heat-Shock Proteins; D003576:Electron Transport Complex IV