Enhanced protein repair and recycling are not correlated with longevity in 15 vertebrate endotherm species.
Identifieur interne : 000950 ( Main/Exploration ); précédent : 000949; suivant : 000951Enhanced protein repair and recycling are not correlated with longevity in 15 vertebrate endotherm species.
Auteurs : Kurtis D. Salway [Canada] ; Melissa M. Page ; Paul A. Faure ; Gary Burness ; Jeffrey A. StuartSource :
- Age (Dordrecht, Netherlands) [ 1574-4647 ] ; 2011.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Proteasome endopeptidase complex, Protéines, Vieillissement.
- Animaux, Homéostasie, Longévité, Vertébrés.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Proteasome Endopeptidase Complex, Proteins.
- metabolism : Aging.
- Animals, Homeostasis, Longevity, Vertebrates.
Abstract
Previous studies have shown that longevity is associated with enhanced cellular stress resistance. This observation supports the disposable soma theory of aging, which suggests that the investment made in cellular maintenance will be proportional to selective pressures to extend lifespan. Maintenance of protein homeostasis is a critical component of cellular maintenance and stress resistance. To test the hypothesis that enhanced protein repair and recycling activities underlie longevity, we measured the activities of the 20S/26S proteasome and two protein repair enzymes in liver, heart and brain tissues of 15 different mammalian and avian species with maximum lifespans (MLSP) ranging from 3 to 30 years. The data set included Snell dwarf mice, in which lifespan is increased by ∼50% compared to their normal littermates. None of these activities in any of the three tissues correlated positively with MLSP. In liver, 20S/26S proteasome and thioredoxin reductase (TrxR) activities correlated negatively with body mass. In brain tissue, TrxR was also negatively correlated with body mass. Glutaredoxin (Grx) activity in brain was negatively correlated with MLSP and this correlation remained after residual analysis to remove the effects of body mass, but was lost when the data were analysed using Felsenstein's independent contrasts. Snell dwarf mice had marginally lower 20S proteasome, TrxR and Grx activities than normal controls in brain, but not heart tissue. Thus, increased longevity is not associated with increased protein repair or proteasomal degradation capacities in vertebrate endotherms.
DOI: 10.1007/s11357-010-9157-5
PubMed: 20567926
PubMed Central: PMC3063641
Affiliations:
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Salway</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Brock University, 500 Glenridge Ave., St. Catharines, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biological Sciences, Brock University, 500 Glenridge Ave., St. Catharines, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Page, Melissa M" sort="Page, Melissa M" uniqKey="Page M" first="Melissa M" last="Page">Melissa M. Page</name></author><author><name sortKey="Faure, Paul A" sort="Faure, Paul A" uniqKey="Faure P" first="Paul A" last="Faure">Paul A. Faure</name></author><author><name sortKey="Burness, Gary" sort="Burness, Gary" uniqKey="Burness G" first="Gary" last="Burness">Gary Burness</name></author><author><name sortKey="Stuart, Jeffrey A" sort="Stuart, Jeffrey A" uniqKey="Stuart J" first="Jeffrey A" last="Stuart">Jeffrey A. Stuart</name></author></analytic><series><title level="j">Age (Dordrecht, Netherlands)</title><idno type="eISSN">1574-4647</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (metabolism)</term><term>Animals (MeSH)</term><term>Homeostasis (MeSH)</term><term>Longevity (MeSH)</term><term>Proteasome Endopeptidase Complex (metabolism)</term><term>Proteins (metabolism)</term><term>Vertebrates (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Homéostasie (MeSH)</term><term>Longévité (MeSH)</term><term>Proteasome endopeptidase complex (métabolisme)</term><term>Protéines (métabolisme)</term><term>Vertébrés (MeSH)</term><term>Vieillissement (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Proteasome Endopeptidase Complex</term><term>Proteins</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aging</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Proteasome endopeptidase complex</term><term>Protéines</term><term>Vieillissement</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Homeostasis</term><term>Longevity</term><term>Vertebrates</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Homéostasie</term><term>Longévité</term><term>Vertébrés</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previous studies have shown that longevity is associated with enhanced cellular stress resistance. This observation supports the disposable soma theory of aging, which suggests that the investment made in cellular maintenance will be proportional to selective pressures to extend lifespan. Maintenance of protein homeostasis is a critical component of cellular maintenance and stress resistance. To test the hypothesis that enhanced protein repair and recycling activities underlie longevity, we measured the activities of the 20S/26S proteasome and two protein repair enzymes in liver, heart and brain tissues of 15 different mammalian and avian species with maximum lifespans (MLSP) ranging from 3 to 30 years. The data set included Snell dwarf mice, in which lifespan is increased by ∼50% compared to their normal littermates. None of these activities in any of the three tissues correlated positively with MLSP. In liver, 20S/26S proteasome and thioredoxin reductase (TrxR) activities correlated negatively with body mass. In brain tissue, TrxR was also negatively correlated with body mass. Glutaredoxin (Grx) activity in brain was negatively correlated with MLSP and this correlation remained after residual analysis to remove the effects of body mass, but was lost when the data were analysed using Felsenstein's independent contrasts. Snell dwarf mice had marginally lower 20S proteasome, TrxR and Grx activities than normal controls in brain, but not heart tissue. Thus, increased longevity is not associated with increased protein repair or proteasomal degradation capacities in vertebrate endotherms.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20567926</PMID><DateCompleted><Year>2011</Year><Month>06</Month><Day>30</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1574-4647</ISSN><JournalIssue CitedMedium="Internet"><Volume>33</Volume><Issue>1</Issue><PubDate><Year>2011</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Age (Dordrecht, Netherlands)</Title><ISOAbbreviation>Age (Dordr)</ISOAbbreviation></Journal><ArticleTitle>Enhanced protein repair and recycling are not correlated with longevity in 15 vertebrate endotherm species.</ArticleTitle><Pagination><MedlinePgn>33-47</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11357-010-9157-5</ELocationID><Abstract><AbstractText>Previous studies have shown that longevity is associated with enhanced cellular stress resistance. This observation supports the disposable soma theory of aging, which suggests that the investment made in cellular maintenance will be proportional to selective pressures to extend lifespan. Maintenance of protein homeostasis is a critical component of cellular maintenance and stress resistance. To test the hypothesis that enhanced protein repair and recycling activities underlie longevity, we measured the activities of the 20S/26S proteasome and two protein repair enzymes in liver, heart and brain tissues of 15 different mammalian and avian species with maximum lifespans (MLSP) ranging from 3 to 30 years. The data set included Snell dwarf mice, in which lifespan is increased by ∼50% compared to their normal littermates. None of these activities in any of the three tissues correlated positively with MLSP. In liver, 20S/26S proteasome and thioredoxin reductase (TrxR) activities correlated negatively with body mass. In brain tissue, TrxR was also negatively correlated with body mass. Glutaredoxin (Grx) activity in brain was negatively correlated with MLSP and this correlation remained after residual analysis to remove the effects of body mass, but was lost when the data were analysed using Felsenstein's independent contrasts. Snell dwarf mice had marginally lower 20S proteasome, TrxR and Grx activities than normal controls in brain, but not heart tissue. 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Faure</name><name sortKey="Page, Melissa M" sort="Page, Melissa M" uniqKey="Page M" first="Melissa M" last="Page">Melissa M. Page</name><name sortKey="Stuart, Jeffrey A" sort="Stuart, Jeffrey A" uniqKey="Stuart J" first="Jeffrey A" last="Stuart">Jeffrey A. Stuart</name></noCountry><country name="Canada"><noRegion><name sortKey="Salway, Kurtis D" sort="Salway, Kurtis D" uniqKey="Salway K" first="Kurtis D" last="Salway">Kurtis D. Salway</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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