Guachalla 2009 Aging (Albany NY): Difference between revisions
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{{Publication | {{Publication | ||
|title=Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B,Jansen-DΓΌrr P,Rudolph KL (2009) | |title=Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B, Jansen-DΓΌrr P, Rudolph KL (2009) SOD2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice. Aging 1: 303-315. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20195488 PMID: 20195488]; [http://www.impactaging.com/papers/v1/n3/full/100030.html PDF] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/20195488 PMID: 20195488]; [http://www.impactaging.com/papers/v1/n3/full/100030.html PDF] | ||
|authors=Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B,Jansen-Duerr P,Rudolph KL | |authors=Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B, Jansen-Duerr P, Rudolph KL | ||
|year=2009 | |year=2009 | ||
|journal=Aging | |journal=Aging | ||
|abstract=Telomere shortening represents a causal factor of cellular senescence. At the same time, several lines of evidenceindicate a pivotal role of oxidative DNA damage for the aging process ''in vivo''. A causal connection between the twoobservations was suggested by experiments showing accelerated telomere shorting under conditions of oxidative stress incultured cells, but has never been studied ''in vivo''. We therefore have analysed whether an increase in mitochondrialderived oxidative stress in response to heterozygous deletion of superoxide dismutase (''Sod2+/β'') would exacerbate agingphenotypes in telomere dysfunctional (''mTercβ/β'') mice. Heterozygous deletion of ''Sod2'' resulted in reduced SOD2 proteinlevels and increased oxidative stress in aging telomere dysfunctional mice, but this did not lead to an increase in basallevels of oxidative nuclear DNA damage, an accumulation of nuclear DNA breaks, or an increased rate of telomereshortening in the mice. Moreover, heterozygous deletion of ''Sod2'' did not accelerate the depletion of stem cells and theimpairment in organ maintenance in aging ''mTercβ/β'' mice. In agreement with these observations, ''Sod2'' haploinsufficiencydid not lead to a further reduction in lifespan of mTercβ/β mice. Together, these results indicate that a decrease in SOD2βdependent antioxidant defence does not exacerbate aging in the context of telomere dysfunction. | |abstract=Telomere shortening represents a causal factor of cellular senescence. At the same time, several lines of evidenceindicate a pivotal role of oxidative DNA damage for the aging process ''in vivo''. A causal connection between the twoobservations was suggested by experiments showing accelerated telomere shorting under conditions of oxidative stress incultured cells, but has never been studied ''in vivo''. We therefore have analysed whether an increase in mitochondrialderived oxidative stress in response to heterozygous deletion of superoxide dismutase (''Sod2+/β'') would exacerbate agingphenotypes in telomere dysfunctional (''mTercβ/β'') mice. Heterozygous deletion of ''Sod2'' resulted in reduced SOD2 proteinlevels and increased oxidative stress in aging telomere dysfunctional mice, but this did not lead to an increase in basallevels of oxidative nuclear DNA damage, an accumulation of nuclear DNA breaks, or an increased rate of telomereshortening in the mice. Moreover, heterozygous deletion of ''Sod2'' did not accelerate the depletion of stem cells and theimpairment in organ maintenance in aging ''mTercβ/β'' mice. In agreement with these observations, ''Sod2'' haploinsufficiencydid not lead to a further reduction in lifespan of mTercβ/β mice. Together, these results indicate that a decrease in SOD2βdependent antioxidant defence does not exacerbate aging in the context of telomere dysfunction. | ||
|keywords=Oxidative stress, Superoxide, Telomere shortening, Aging, DNA damage, SOD2, Free radicals, Stem cells | |keywords=Oxidative stress, Superoxide, Telomere shortening, Aging, DNA damage, SOD2, Free radicals, Stem cells | ||
|mipnetlab=AT_Innsbruck_Jansen Duerr P | |mipnetlab=AT_Innsbruck_Jansen-Duerr P | ||
}} | }} | ||
{{Labeling | {{Labeling |
Revision as of 13:20, 19 April 2012
Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B, Jansen-DΓΌrr P, Rudolph KL (2009) SOD2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice. Aging 1: 303-315. |
Β» PMID: 20195488; PDF
Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B, Jansen-Duerr P, Rudolph KL (2009) Aging
Abstract: Telomere shortening represents a causal factor of cellular senescence. At the same time, several lines of evidenceindicate a pivotal role of oxidative DNA damage for the aging process in vivo. A causal connection between the twoobservations was suggested by experiments showing accelerated telomere shorting under conditions of oxidative stress incultured cells, but has never been studied in vivo. We therefore have analysed whether an increase in mitochondrialderived oxidative stress in response to heterozygous deletion of superoxide dismutase (Sod2+/β) would exacerbate agingphenotypes in telomere dysfunctional (mTercβ/β) mice. Heterozygous deletion of Sod2 resulted in reduced SOD2 proteinlevels and increased oxidative stress in aging telomere dysfunctional mice, but this did not lead to an increase in basallevels of oxidative nuclear DNA damage, an accumulation of nuclear DNA breaks, or an increased rate of telomereshortening in the mice. Moreover, heterozygous deletion of Sod2 did not accelerate the depletion of stem cells and theimpairment in organ maintenance in aging mTercβ/β mice. In agreement with these observations, Sod2 haploinsufficiencydid not lead to a further reduction in lifespan of mTercβ/β mice. Together, these results indicate that a decrease in SOD2βdependent antioxidant defence does not exacerbate aging in the context of telomere dysfunction. β’ Keywords: Oxidative stress, Superoxide, Telomere shortening, Aging, DNA damage, SOD2, Free radicals, Stem cells
β’ O2k-Network Lab: AT_Innsbruck_Jansen-Duerr P
Labels:
Stress:Aging; Senescence"Aging; Senescence" 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., Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" 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: Mouse Tissue;cell: Neurons; Brain"Neurons; Brain" 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: Uncoupling protein 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., Redox State"Redox State" 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