Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei.

Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei. Research Abstract Details 

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Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei. Abstract Text:

Esther E Dupont-Versteegden,Beau A Strotman,Cathy M Gurley,Dana Gaddy,Micheal Knox,James D Fluckey,Charlotte A Peterson,

Skeletal muscle atrophy is associated with an increase in apoptosis, and we showed previously that endonuclease G (EndoG) is localized to nuclei following unloading. The goal of this study was to determine whether the onset of apoptosis in response to disuse was consistent with the hypothesis that EndoG is involved in myofiber nuclear loss. Atrophy was induced by hindlimb suspension for 12 h or 1, 2, 4 and 7 days in 6-mo-old rats. Soleus myofiber cross-sectional area decreased significantly by 2 days, whereas muscle mass and muscle-to-body mass ratio decreased by 4 and 7 days, respectively. By contrast, a significant increase in apoptosis, evidenced by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive nuclei, occurred as early as 12 h after suspension, preceding the elevation in muscle atrophy F-box gene expression. The early increase in apoptosis appeared to be specific to myofiber nuclei, whereas TUNEL-positive interstitial cells did not become significantly elevated until 2 days after suspension. Furthermore, TUNEL-positive myofiber nuclei colocalized with EndoG as early as 12 h after suspension, and no such localization was observed in interstitial cells. Although no significant change in total activated caspase-3, -7, or -12 protein abundance was apparent, activated caspase-3 was expressed in interstitial cells undergoing apoptosis, some of which were endothelial cells. These data indicate that apoptosis is an early, and therefore possibly causative, event in the process of muscle atrophy, and that EndoG nuclear translocation is specific for myofiber nuclear apoptosis, whereas interstitial cells may undergo apoptosis via a more classical, caspase-dependent pathway.

Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei. Publishing Authors By Initials

EE Dupont-Versteegden,BA Strotman,CM Gurley,D Gaddy,M Knox,JD Fluckey,CA Peterson,

For similar animals: chordata: vertebrates: mammals: rodentia: muridae: murinae: rats: rats, sprague-dawley research abstracts see: animals: chordata: vertebrates: mammals: rodentia: muridae: murinae: rats: rats, sprague-dawley research

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Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Regulatory, integr

VOLUME: 291

Page Numbers: R1730-40

Journal Abbreviation: Am. J. Physiol. Regul. Integr.

ISSN: 0363-6119

DAY: 27

MONTH: 07

YEAR: 2006

Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901230

Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei. Keywords Mesh Terms:

KEYWORDS: Rats, Sprague-Dawley

MESH TERMS: pathology

Chemical & Substance for Abstract: Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei. Information

Substance Name: endonuclease G

Registry Number: EC 3.1.21.-

Grant and Affiliation Information for Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei.

AFFILIATION: Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA. eedupo2@email.uky.edu

Country: United States

AGENCY: United States NCRR

GRANT: P20 RR 16460

ACRONYM: RR

MEDLINETA: Am J Physiol Regul Integr Comp

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