Gnaiger 2000 Transpl Int

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
Gnaiger E, Kuznetsov AV, Rieger G, Amberger A, Fuchs A, Stadlmann S, Eberl T, Margreiter R (2000) Mitochondrial defects by intracellular calcium overload versus endothelial cold ischemia/reperfusion injury. Transpl Int 13:555-7.

» PMID: 11112072

Gnaiger E, Kuznetsov AV, Rieger G, Amberger A, Fuchs A, Stadlmann S, Eberl T, Margreiter R (2000) Transpl Int

Abstract: Questions as to the critical stress factor and primary targets of cold ischemia/reperfusion (CIR) injury were addressed by comparing mitochondrial defects caused by (1) CIR injury and (2) intracellular Ca2+ overload. CIR was simulated in transformed human umbilical vein endothelial cell cultures (tEC) by 8 h cold anoxia in University of Wisconsin solution and reoxygenation at 37 °C. Intracellular Ca2+ concentrations were changed by permeabilization of suspended cells with digitonin in culture medium (RPMI, 0.4 mM Ca2+). Binding of free Ca2+ by ethylene glycol-bis(β-aminoethylether)- N,N,N',N'-tetraacetic acid in RPMI or mitochondrial incubation medium served as controls. Extracellular Ca2+ protected the cell membrane against permeabilization. Mitochondrial functions were determined before and after permeabilization of the cell membrane. After CIR, mitochondrial respiratory capacity declined, but oxygen consumption remained coupled to adenosine triphosphate (ATP) production. In contrast, Ca2+ overload caused uncoupling of mitochondrial respiration. High intracellular Ca2+ overload, therefore, does not reproduce cold ischemia/ reperfusion injury in endothelial cells.

Keywords: Ischemia/reperfusion injury, Endothelial cells, Plasma membrane, Intracellular Ca2+, Mitochondrial respiratory chain, Oxidative phosphorylation

O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros

Labels: MiParea: Respiration 

Stress:Ischemia-reperfusion, Oxidative stress;RONS  Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell, HUVEC  Preparation: Intact cells, Permeabilized cells, Oxidase;biochemical oxidation 

Regulation: Calcium  Coupling state: ROUTINE, OXPHOS 

HRR: Oxygraph-2k