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Article: Aging alters the reduction of pro-apoptotic signaling in response to loading-induced hypertrophy

TitleAging alters the reduction of pro-apoptotic signaling in response to loading-induced hypertrophy
Authors
KeywordsAging
Muscle hypertrophy
XIAP
Apoptosis
AIF
Repressors to apoptosis
Sarcopenia
Issue Date2006
Citation
Experimental Gerontology, 2006, v. 41, n. 2, p. 175-188 How to Cite?
AbstractThis study tested the hypothesis that loading decreased apoptosis in skeletal muscle in an aging-dependent fashion. One wing of young and aged Japanese quails was loaded for 7 or 21 days to induce hypertrophy. The contralateral wing served as the intra-animal control. Loading increased fast-twitch quail patagialis muscle mass by 28 and 49%, after 7 or 21 days of loading, respectively in young adult birds. Muscle mass was not elevated after 7 days of loading, but increased by 29% after 21 days of loading in aged birds. Seven days of loading reduced DNA fragmentation and cytosolic accumulation of cytochrome c in muscles from young birds but not in muscles from aged birds. ARC protein content was lower and H 2 O 2 content was higher in muscles from aged birds following 7 days of loading. The mitochondria-free cytosolic protein fraction from muscles loaded for 7 days had 41 and 29% lower AIF content than control muscles in young and aged birds, respectively. XIAP, an apoptotic suppressor protein increased after 7 days of loading in muscles from young adult but not aged birds. Our results suggest that loading suppresses pro-apoptotic signaling in quail muscle but aging delays or attenuates these anti-apoptotic changes. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/244079
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 1.051
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSiu, Parco M.-
dc.contributor.authorAlway, Stephen E.-
dc.date.accessioned2017-08-31T08:55:59Z-
dc.date.available2017-08-31T08:55:59Z-
dc.date.issued2006-
dc.identifier.citationExperimental Gerontology, 2006, v. 41, n. 2, p. 175-188-
dc.identifier.issn0531-5565-
dc.identifier.urihttp://hdl.handle.net/10722/244079-
dc.description.abstractThis study tested the hypothesis that loading decreased apoptosis in skeletal muscle in an aging-dependent fashion. One wing of young and aged Japanese quails was loaded for 7 or 21 days to induce hypertrophy. The contralateral wing served as the intra-animal control. Loading increased fast-twitch quail patagialis muscle mass by 28 and 49%, after 7 or 21 days of loading, respectively in young adult birds. Muscle mass was not elevated after 7 days of loading, but increased by 29% after 21 days of loading in aged birds. Seven days of loading reduced DNA fragmentation and cytosolic accumulation of cytochrome c in muscles from young birds but not in muscles from aged birds. ARC protein content was lower and H 2 O 2 content was higher in muscles from aged birds following 7 days of loading. The mitochondria-free cytosolic protein fraction from muscles loaded for 7 days had 41 and 29% lower AIF content than control muscles in young and aged birds, respectively. XIAP, an apoptotic suppressor protein increased after 7 days of loading in muscles from young adult but not aged birds. Our results suggest that loading suppresses pro-apoptotic signaling in quail muscle but aging delays or attenuates these anti-apoptotic changes. © 2005 Elsevier Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofExperimental Gerontology-
dc.subjectAging-
dc.subjectMuscle hypertrophy-
dc.subjectXIAP-
dc.subjectApoptosis-
dc.subjectAIF-
dc.subjectRepressors to apoptosis-
dc.subjectSarcopenia-
dc.titleAging alters the reduction of pro-apoptotic signaling in response to loading-induced hypertrophy-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.exger.2005.11.004-
dc.identifier.pmid16377111-
dc.identifier.scopuseid_2-s2.0-31544434882-
dc.identifier.volume41-
dc.identifier.issue2-
dc.identifier.spage175-
dc.identifier.epage188-
dc.identifier.isiWOS:000235423900009-
dc.identifier.issnl0531-5565-

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