Difference between revisions of "Dikov 2010 Exp Gerontol"
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{{Publication | {{Publication | ||
|title=Dikov D, Aulbach A, Muster B, Dröse S, Jendrach M, Bereiter-Hahn J (2010) Do UCP2 and mild uncoupling improve longevity? Exp. Gerontol. 45(7-8):586-595. | |title=Dikov D, Aulbach A, Muster B, Dröse S, Jendrach M, Bereiter-Hahn J (2010) Do UCP2 and mild uncoupling improve longevity? Exp. Gerontol. 45(7-8):586-595. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20332018 PMID: 20332018] | |||
|authors=Dikov D, Aulbach A, Muster B, Droese S, Jendrach M, Bereiter-Hahn J | |authors=Dikov D, Aulbach A, Muster B, Droese S, Jendrach M, Bereiter-Hahn J | ||
|year=2010 | |year=2010 | ||
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|abstract=Mild uncoupling of mitochondrial respiration is considered to prolong life span of organisms by reducing the production of reactive oxygen species (ROS). Experimental evidence against this hypothesis has been brought forward by premature senescence in cell cultures treated with uncouplers. Exposing HUVEC to a mixture of nutritionally important fatty acids (oil extract of chicken yolk) mild uncoupling with "naturally acting substances" was performed. This treatment also resulted in premature senescence although ROS production did not increase. Fatty acids activate uncoupling proteins (UCP) in the inner mitochondrial membrane. UCP2 expression proved to be sensitive to the presence of fatty acids but remains unchanged during the ageing process. UCP3 expression in senescent HUVEC and avUCP expression in senescent CEF were considerably less than in young cultures. No indication for protonophoric reduction of mitochondrial membrane potential was found in UCP2 overexpressing HeLa cells and only little in HUVEC. ROS levels increased instead of being reduced in these cells. Stable transfection with UCP2-GFP was possible only in chick embryo fibroblasts and HeLa cells and resulted in decreased proliferation. Stable transfection of HUVEC with UCP2-GFP resulted in death of cultures within one or two weeks. The reason for this behaviour most probably is apoptosis preceded by mitochondrial fragmentation and loss of membrane potential. | |abstract=Mild uncoupling of mitochondrial respiration is considered to prolong life span of organisms by reducing the production of reactive oxygen species (ROS). Experimental evidence against this hypothesis has been brought forward by premature senescence in cell cultures treated with uncouplers. Exposing HUVEC to a mixture of nutritionally important fatty acids (oil extract of chicken yolk) mild uncoupling with "naturally acting substances" was performed. This treatment also resulted in premature senescence although ROS production did not increase. Fatty acids activate uncoupling proteins (UCP) in the inner mitochondrial membrane. UCP2 expression proved to be sensitive to the presence of fatty acids but remains unchanged during the ageing process. UCP3 expression in senescent HUVEC and avUCP expression in senescent CEF were considerably less than in young cultures. No indication for protonophoric reduction of mitochondrial membrane potential was found in UCP2 overexpressing HeLa cells and only little in HUVEC. ROS levels increased instead of being reduced in these cells. Stable transfection with UCP2-GFP was possible only in chick embryo fibroblasts and HeLa cells and resulted in decreased proliferation. Stable transfection of HUVEC with UCP2-GFP resulted in death of cultures within one or two weeks. The reason for this behaviour most probably is apoptosis preceded by mitochondrial fragmentation and loss of membrane potential. | ||
|keywords=Uncoupler, Longevity, ROS,UCP2/3,Fatty acids, Mitochondrial membrane potential, HUVEC | |keywords=Uncoupler, Longevity, ROS,UCP2/3,Fatty acids, Mitochondrial membrane potential, HUVEC | ||
| | |discipline=Mitochondrial Physiology | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
| | |instruments=Oxygraph-2k | ||
|injuries=RONS; Oxidative Stress | |injuries=RONS; Oxidative Stress | ||
|organism=Human | |organism=Human | ||
|tissues=Endothelial; Epithelial; Mesothelial Cell | |tissues=Endothelial; Epithelial; Mesothelial Cell | ||
|preparations=Intact Cell; Cultured; Primary | |||
|enzymes=Uncoupler Protein | |||
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential | |topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential | ||
| | |discipline=Mitochondrial Physiology | ||
}} | }} | ||
'''Abbreviations''': mtΔψ, mitochondrial inner membrane potential; CEF, chick embryo fibroblasts; DASPMI, di-aminostyryl-methyl-pyrimidinium iodine; DHE, dihydro-ethidium; FCCP, carbonyl cyanid-p-triflouromethoxyphenylhydrazin; HUVEC, human umbilical vein endothelial cells; ROS, reactive oxygen species; TMRE, tetramethyl-rhodamine-ethylester | '''Abbreviations''': mtΔψ, mitochondrial inner membrane potential; CEF, chick embryo fibroblasts; DASPMI, di-aminostyryl-methyl-pyrimidinium iodine; DHE, dihydro-ethidium; FCCP, carbonyl cyanid-p-triflouromethoxyphenylhydrazin; HUVEC, human umbilical vein endothelial cells; ROS, reactive oxygen species; TMRE, tetramethyl-rhodamine-ethylester | ||
Revision as of 09:27, 8 September 2011
| Dikov D, Aulbach A, Muster B, Dröse S, Jendrach M, Bereiter-Hahn J (2010) Do UCP2 and mild uncoupling improve longevity? Exp. Gerontol. 45(7-8):586-595. |
Dikov D, Aulbach A, Muster B, Droese S, Jendrach M, Bereiter-Hahn J (2010) Exp. Gerontol.
Abstract: Mild uncoupling of mitochondrial respiration is considered to prolong life span of organisms by reducing the production of reactive oxygen species (ROS). Experimental evidence against this hypothesis has been brought forward by premature senescence in cell cultures treated with uncouplers. Exposing HUVEC to a mixture of nutritionally important fatty acids (oil extract of chicken yolk) mild uncoupling with "naturally acting substances" was performed. This treatment also resulted in premature senescence although ROS production did not increase. Fatty acids activate uncoupling proteins (UCP) in the inner mitochondrial membrane. UCP2 expression proved to be sensitive to the presence of fatty acids but remains unchanged during the ageing process. UCP3 expression in senescent HUVEC and avUCP expression in senescent CEF were considerably less than in young cultures. No indication for protonophoric reduction of mitochondrial membrane potential was found in UCP2 overexpressing HeLa cells and only little in HUVEC. ROS levels increased instead of being reduced in these cells. Stable transfection with UCP2-GFP was possible only in chick embryo fibroblasts and HeLa cells and resulted in decreased proliferation. Stable transfection of HUVEC with UCP2-GFP resulted in death of cultures within one or two weeks. The reason for this behaviour most probably is apoptosis preceded by mitochondrial fragmentation and loss of membrane potential. • Keywords: Uncoupler, Longevity, ROS, UCP2/3, Fatty acids, Mitochondrial membrane potential, HUVEC
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. Enzyme: Uncoupler Protein"Uncoupler Protein" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" 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.
HRR: Oxygraph-2k
Abbreviations: mtΔψ, mitochondrial inner membrane potential; CEF, chick embryo fibroblasts; DASPMI, di-aminostyryl-methyl-pyrimidinium iodine; DHE, dihydro-ethidium; FCCP, carbonyl cyanid-p-triflouromethoxyphenylhydrazin; HUVEC, human umbilical vein endothelial cells; ROS, reactive oxygen species; TMRE, tetramethyl-rhodamine-ethylester
