The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
J C Jiang - One of the best experts on this subject based on the ideXlab platform.
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Distinct roles of processes modulated by histone deacetylases Rpd3p, Hda1p, and Sir2p in life extension by Caloric Restriction in yeast
Experimental Gerontology, 2002Co-Authors: J C Jiang, J Wawryn, H.m.c Shantha Kumara, S M JazwinskiAbstract:Caloric Restriction has been demonstrated to extend life span and postpone aging in a variety of species. The recent extension of the Caloric Restriction paradigm to yeast places the emphasis of the search for the longevity effectors at the cellular level. To narrow the range of potential effectors of the Caloric Restriction response, we have examined the effects of the histone deacetylases Rpd3p, Hda1p, and Sir2p, which have distinguishable but partially overlapping influences on global patterns of gene expression, on the life extension afforded by Caloric Restriction. Deletion of the RPD3 gene extended life span, and there was no additive effect of Caloric Restriction. Deletion of HDA1 had no effect of its own on longevity but acted synergistically with Caloric Restriction to increase life span. SIR2 deletion shortened life span but did not prevent extension of life span by Caloric Restriction. The results suggest that Rpd3p affects both processes that play an obligate and those that play a synergistic role in life extension by Caloric Restriction, while Hda1p and Sir2p affect processes that are not the obligate longevity effectors of Caloric Restriction but instead synergize with them, although in opposite directions. From the known patterns of gene expression elicited by rpd3Δ, hda1Δ, and sir2Δ, we propose that the major longevity effectors of Caloric Restriction in yeast involve carbohydrate/energy metabolism and mitochondrial function.
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Distinct roles of processes modulated by histone deacetylases Rpd3p, Hda1p, and Sir2p in life extension by Caloric Restriction in yeast.
Experimental gerontology, 2002Co-Authors: J C Jiang, J Wawryn, H M C Shantha Kumara, S M JazwinskiAbstract:Caloric Restriction has been demonstrated to extend life span and postpone aging in a variety of species. The recent extension of the Caloric Restriction paradigm to yeast places the emphasis of the search for the longevity effectors at the cellular level. To narrow the range of potential effectors of the Caloric Restriction response, we have examined the effects of the histone deacetylases Rpd3p, Hda1p, and Sir2p, which have distinguishable but partially overlapping influences on global patterns of gene expression, on the life extension afforded by Caloric Restriction. Deletion of the RPD3 gene extended life span, and there was no additive effect of Caloric Restriction. Deletion of HDA1 had no effect of its own on longevity but acted synergistically with Caloric Restriction to increase life span. SIR2 deletion shortened life span but did not prevent extension of life span by Caloric Restriction. The results suggest that Rpd3p affects both processes that play an obligate and those that play a synergistic role in life extension by Caloric Restriction, while Hda1p and Sir2p affect processes that are not the obligate longevity effectors of Caloric Restriction but instead synergize with them, although in opposite directions. From the known patterns of gene expression elicited by rpd3delta, hda1delta, and sir2delta, we propose that the major longevity effectors of Caloric Restriction in yeast involve carbohydrate/energy metabolism and mitochondrial function.
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an intervention resembling Caloric Restriction prolongs life span and retards aging in yeast
The FASEB Journal, 2000Co-Authors: J C Jiang, Ewa Jaruga, Marina V Repnevskaya, Michal S JazwinskiAbstract:The yeast Saccharomyces cerevisiae has a finite life span that is measured by the number of daughter cells an individual produces. The 20 genes known to determine yeast life span appear to function in more than one pathway, implicating a variety of physiological processes in yeast longevity. Less attention has been focused on environmental effects on yeast aging. We have examined the role that nutritional status plays in determining yeast life span. Reduction of the glucose concentration in the medium led to an increase in life span and to a delay in appearance of an aging phenotype. The increase in life span was the more extensive the lower the glucose levels. Life extension was also elicited by decreasing the amino acids content of the medium. This suggests that it is the decline in calories and not a particular nutrient that is responsible, in striking similarity to the effect on aging of Caloric Restriction in mammals. The Caloric Restriction effect did not require the induction of the retrograde response pathway, which signals the functional status of the mitochondrion and determines longevity. Furthermore, deletion of RTG3, a downstream mediator in this pathway, and Caloric Restriction had an additive effect, resulting in the largest increase (123%) in longevity described thus far in yeast. Thus, retrograde response and Caloric Restriction operate along distinct pathways in determining yeast longevity. These pathways may be exclusive, at least in part. This provides evidence for multiple mechanisms of metabolic control in yeast aging. Inasmuch as Caloric Restriction lowers blood glucose levels, this study raises the possibility that reduced glucose alters aging at the cellular level in mammals.
Jason E. Fish - One of the best experts on this subject based on the ideXlab platform.
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Cardioprotective Signature of Short-Term Caloric Restriction.
PloS one, 2015Co-Authors: Hossein Noyan, Omar El-mounayri, Ruth Isserlin, Sara Arab, Abdul Momen, Henry S. Cheng, Talat Afroze, Jason E. FishAbstract:Objective To understand the molecular pathways underlying the cardiac preconditioning effect of short-term Caloric Restriction (CR).
S M Jazwinski - One of the best experts on this subject based on the ideXlab platform.
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Distinct roles of processes modulated by histone deacetylases Rpd3p, Hda1p, and Sir2p in life extension by Caloric Restriction in yeast
Experimental Gerontology, 2002Co-Authors: J C Jiang, J Wawryn, H.m.c Shantha Kumara, S M JazwinskiAbstract:Caloric Restriction has been demonstrated to extend life span and postpone aging in a variety of species. The recent extension of the Caloric Restriction paradigm to yeast places the emphasis of the search for the longevity effectors at the cellular level. To narrow the range of potential effectors of the Caloric Restriction response, we have examined the effects of the histone deacetylases Rpd3p, Hda1p, and Sir2p, which have distinguishable but partially overlapping influences on global patterns of gene expression, on the life extension afforded by Caloric Restriction. Deletion of the RPD3 gene extended life span, and there was no additive effect of Caloric Restriction. Deletion of HDA1 had no effect of its own on longevity but acted synergistically with Caloric Restriction to increase life span. SIR2 deletion shortened life span but did not prevent extension of life span by Caloric Restriction. The results suggest that Rpd3p affects both processes that play an obligate and those that play a synergistic role in life extension by Caloric Restriction, while Hda1p and Sir2p affect processes that are not the obligate longevity effectors of Caloric Restriction but instead synergize with them, although in opposite directions. From the known patterns of gene expression elicited by rpd3Δ, hda1Δ, and sir2Δ, we propose that the major longevity effectors of Caloric Restriction in yeast involve carbohydrate/energy metabolism and mitochondrial function.
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Distinct roles of processes modulated by histone deacetylases Rpd3p, Hda1p, and Sir2p in life extension by Caloric Restriction in yeast.
Experimental gerontology, 2002Co-Authors: J C Jiang, J Wawryn, H M C Shantha Kumara, S M JazwinskiAbstract:Caloric Restriction has been demonstrated to extend life span and postpone aging in a variety of species. The recent extension of the Caloric Restriction paradigm to yeast places the emphasis of the search for the longevity effectors at the cellular level. To narrow the range of potential effectors of the Caloric Restriction response, we have examined the effects of the histone deacetylases Rpd3p, Hda1p, and Sir2p, which have distinguishable but partially overlapping influences on global patterns of gene expression, on the life extension afforded by Caloric Restriction. Deletion of the RPD3 gene extended life span, and there was no additive effect of Caloric Restriction. Deletion of HDA1 had no effect of its own on longevity but acted synergistically with Caloric Restriction to increase life span. SIR2 deletion shortened life span but did not prevent extension of life span by Caloric Restriction. The results suggest that Rpd3p affects both processes that play an obligate and those that play a synergistic role in life extension by Caloric Restriction, while Hda1p and Sir2p affect processes that are not the obligate longevity effectors of Caloric Restriction but instead synergize with them, although in opposite directions. From the known patterns of gene expression elicited by rpd3delta, hda1delta, and sir2delta, we propose that the major longevity effectors of Caloric Restriction in yeast involve carbohydrate/energy metabolism and mitochondrial function.
Hossein Noyan - One of the best experts on this subject based on the ideXlab platform.
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Cardioprotective Signature of Short-Term Caloric Restriction.
PloS one, 2015Co-Authors: Hossein Noyan, Omar El-mounayri, Ruth Isserlin, Sara Arab, Abdul Momen, Henry S. Cheng, Talat Afroze, Jason E. FishAbstract:Objective To understand the molecular pathways underlying the cardiac preconditioning effect of short-term Caloric Restriction (CR).
George S. Roth - One of the best experts on this subject based on the ideXlab platform.
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Caloric Restriction Mimetics
Methods in molecular biology (Clifton N.J.), 2007Co-Authors: Mark A. Lane, George S. Roth, Donald K. IngramAbstract:Caloric Restriction remains the only nongenetic intervention that has been consistently and reproducibly shown to extend both average and maximal lifespan in a wide variety of species. If shown to be applicable to human aging, it is unlikely that most people would be able to maintain the 30-40% reduction in food intake apparently required for this intervention. Therefore, an alternative approach is needed. We first proposed the concept of Caloric Restriction (CR) mimetics in 1998. Since its introduction, this research area has witnessed a significant expansion of interest in academic, government, and private sectors. CR mimetics target alteration of pathways of energy metabolism to potentially mimic the beneficial health-promoting and anti-aging effects of CR without the need to reduce food intake significantly. To date, a number of candidate CR mimetics including glycolytic inhibitors, antioxidants and specific gene-modulators have been investigated and appear to validate the potential of this approach.
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Caloric Restriction and Caloric Restriction mimetics: current status and promise for the future.
Journal of the American Geriatrics Society, 2005Co-Authors: George S. RothAbstract:Dietary Caloric Restriction is the most reproducible means of extending longevity and maintaining health and vitality. It has been shown to be relevant to a wide rage of species, including primates. Examination of key markers of the Calorically restricted phenotype, such as plasma insulin, dehydroepiandrosterone sulfate, and body temperature, suggest that they may predict longevity in humans as well. However, most people would be unwilling or unable to adopt the 30% to 40% reduction in food intake necessary to achieve optimal health and longevity benefits. For this reason, a number of laboratories are pursuing Caloric Restriction mimetics: ways to achieve the benefits of Restriction without eating less. This approach will undoubtedly remain a major focus of biogerontology for the foreseeable future.
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The Effect of Caloric Restriction on Glycation and Glycoxidation in Skin Collagen of Nonhuman Primates
The journals of gerontology. Series A Biological sciences and medical sciences, 2003Co-Authors: David R. Sell, Mark A. Lane, George S. Roth, Donald K. Ingram, Mark E. Obrenovich, Julie A. Mattison, April M. Handy, Richard G. Cutler, Vincent M. MonnierAbstract:The accumulation of Maillard reaction products increases with age in long-lived proteins and can be retarded by Caloric Restriction. Here we determined whether Caloric Restriction inhibits formation of glycation and glycoxidation products in skin collagen of squirrel and rhesus monkeys between 1990-1997. Restricted monkeys (n = 11, n = 30, respectively) were maintained at 70% of Caloric intake of controls (n = 25, n = 32, respectively). Glycation was assessed by furosine and glycoxidation by pentosidine and carboxymethyl-lysine. With age, the rate of furosine formation moderately but nonsignificantly (p >.05) increased in both control monkey groups. It significantly (p =.011) decreased in the Caloric-restricted rhesus, but not squirrel monkeys. Caloric Restriction did not significantly decrease the pentosidine or carboxymethyl-lysine rates in either species of monkeys. These results suggest that Caloric Restriction, when maintained long-term in nonhuman primates, tends to decrease glycation, but not glycoxidation.
