Cited by 24Muscle Physiology and DisordersGenetics, Aging, and Longevity in Model OrganismsCell death mechanisms and regulation

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

Siu, Parco M., Alway, Stephen E.·2006·Experimental Gerontology

Abstract

This 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 H2O2 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.

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Crossref · 10.1016/j.exger.2005.11.004

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  • Apoptosis signaling has been reported in muscle and neuronal cells of aged rodents and humans.

    “Apoptosis signaling has been reported in muscle and neuronal cells of aged rodents (4, 7, 26, 34, 47, 77, 88, 130), and humans (44, 145).”

    From Mitochondria initiate and regulate sarcopenia (2017) · cites this paper as [130]

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Authors
Siu, P. M., & Alway, S. E.
Affiliations
West Virginia University (US)
Corresponding author
Alway, Stephen E.
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
2006-02
Volume
41
Issue
2
Pages
175-188
ISSN
0531-5565 (ISSN-L)
OpenAlex
W2059959902
Cited by
24
References
82
Citations by year
2023: 1 · 2018: 3 · 2017: 2 · 2014: 1 · 2012: 1
FWCI
0.38
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Gerontology (publishedVersion)
  • PubMed (publishedVersion)
  • The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
Funders
National Institute on Aging (R01AG021530)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
aging, muscle hypertrophy, mechanical loading, apoptosis, skeletal muscle, Japanese quail, fast-twitch muscle, cytochrome c, apoptosis-inducing factor, XIAP, Arc protein, hydrogen peroxide, mitochondrial proteins, DNA fragmentation
MeSH terms
Aging, Animals, Coturnix, Cytosol, Hydrogen Peroxide, Hypertrophy, Male, Time Factors, Signal Transduction, Biomarkers, Weight-Bearing, Apoptosis, Muscle, Skeletal, Muscle Fibers, Fast-Twitch, In Situ Nick-End Labeling, Cytochromes c, Apoptosis Regulatory Proteins, Apoptosis Inducing Factor, X-Linked Inhibitor of Apoptosis Protein

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