Difference between revisions of "Gnaiger 2000 Transpl Int"
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{{Publication | {{Publication | ||
|title=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: 555-557. | |title=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: 555-557. | ||
|authors=Gnaiger E, Kuznetsov AV, Rieger G, Amberger A, Fuchs A, Stadlmann S, Eberl T, Margreiter R Β | |authors=Gnaiger E, Kuznetsov AV, Rieger G, Amberger A, Fuchs A, Stadlmann S, Eberl T, Margreiter R | ||
|year=2000 | |year=2000 | ||
|journal=Transpl. Int. | |journal=Transpl. Int. | ||
|mipnetlab=AT_Innsbruck_GnaigerE | |mipnetlab=AT_Innsbruck_GnaigerE | ||
|abstract=Questions as to the critical stress factor and primary targets of cold ischemia/reperfusion (CIR) injury were addressed by comparing | |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 | ||
mitochondrial defects caused by (1) CIR injury and (2) intracellular Ca2+ overload. CIR was simulated in transformed human umbilical vein | at 37 οΏ½C. 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(baminoethylether)- N,N,N',N'-tetraacetic acid in RPMI or mitochondrial incubation medium served as | ||
endothelial cell cultures (tEC) by 8 h cold anoxia in University of Wisconsin solution and reoxygenation | 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, | ||
at 37 οΏ½C. Intracellular Ca2+ concentrations were changed by permeabilization of suspended cells with digitonin in culture medium | does not reproduce cold ischemia/ reperfusion injury in endothelial cells. | ||
(RPMI, 0.4 mM Ca2+). Binding of free Ca2+ by ethylene glycol-bis(baminoethylether)- N,N,N',N'-tetraacetic | |keywords=Ischemia/reperfusion injury , Endothelial cells,Β Plasma membrane,Β Intracellular Ca2+, Mitochondrial respiratory chain, Oxidative phosphorylation | ||
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 | |||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/11112072 PMID: 11112072] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/11112072 PMID: 11112072] | ||
}} | }} |
Revision as of 17:36, 13 September 2010
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: 555-557. |
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 οΏ½C. 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(baminoethylether)- 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. β’ Keywords: Ischemia/reperfusion injury, Endothelial cells, Plasma membrane, Intracellular Ca2+, Mitochondrial respiratory chain, Oxidative phosphorylation
β’ O2k-Network Lab: AT_Innsbruck_GnaigerE
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Endothelial; Epithelial; Mesothelial Cell"Endothelial; Epithelial; Mesothelial Cell" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. Preparation: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Coupling; Membrane Potential"Coupling; Membrane Potential" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Ion Homeostasis"Ion Homeostasis" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k