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dc.contributor.author김종희-
dc.date.accessioned2016-12-09T01:37:04Z-
dc.date.available2016-12-09T01:37:04Z-
dc.date.issued2015-05-
dc.identifier.citationJOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES, v. 70, NO 5, Page. 533-544en_US
dc.identifier.issn1079-5006-
dc.identifier.issn1758-535X-
dc.identifier.urihttp://biomedgerontology.oxfordjournals.org/content/70/5/533-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/24762-
dc.description.abstractContractility of the heart is impaired with advancing age via mechanical remodeling, as myocytes are lost through apoptosis and collagenous fibers accumulate. Exercise training confers protection against fibrosis and apoptosis in the aging heart, but the mechanisms remain poorly understood. We recently reported that exercise training elevates Mn isoform of superoxide dismutase (MnSOD) in the aging heart, concomitant with reduction in oxidative stress and fibrosis. Here, we tested the hypothesis that overexpression of MnSOD would be causal in protection against fibrosis and apoptosis in the aging heart. Hearts were extracted from young (8 months) wild-type, young mice overexpressing the Sod2 (MnSOD) gene, old (28 months) wild-type, and old transgenic mice. Left ventricle MnSOD protein levels were elevated in young mice overexpressing the Sod2 (MnSOD) gene and old transgenic mice. MnSODTg mice exhibited lower oxidative stress (total hydroperoxides, 4-hydroxynonenal, and 8-isoprostane) in the old group. Age-related cardiac remodeling and fibrosis was mitigated in MnSOD Tg mice with reductions in extramyocyte space (-65%), collagen-I, and transforming growth factor-beta. Pro-apoptotic markers Bax (-38%) and caspase-3 cleavage (-41%) were reduced and apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive nuclei, DNA laddering) was mitigated in MnSOD Tg hearts compared with old wild-type. We conclude that MnSOD elevation is indeed protective against oxidative stress, fibrosis, and apoptosis in the aging heart.en_US
dc.description.sponsorshipThis study was supported by the American Heart Association (0555064Y and 0855158F), National Institutes of Health (AR054084), National Aeronautics and Space Administration (NASA; NNX12AR62G), and the Sydney and J. L. Huffines Institute for Sports Medicine.en_US
dc.language.isoenen_US
dc.publisherOXFORD UNIV PRESS INCen_US
dc.subjectAgingen_US
dc.subjectHearten_US
dc.subjectSuperoxide dismutaseen_US
dc.subjectOxidative stressen_US
dc.subjectFibrosisen_US
dc.titleMnSOD Overexpression Reduces Fibrosis and Pro-Apoptotic Signaling in the Aging Mouse Hearten_US
dc.typeArticleen_US
dc.relation.no5-
dc.relation.volume70-
dc.identifier.doi10.1093/gerona/glu090-
dc.relation.page533-544-
dc.relation.journalJOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES-
dc.contributor.googleauthorKwak, Hyo-Bum-
dc.contributor.googleauthorLee, Yang-
dc.contributor.googleauthorKim, Jong-Hee-
dc.contributor.googleauthorVan Remmen, Holly-
dc.contributor.googleauthorRichardson, Arlan G.-
dc.contributor.googleauthorLawler, John M.-
dc.relation.code2015000490-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF ART AND PHYSICAL EDUCATION[S]-
dc.sector.departmentDEPARTMENT OF PHYSICAL EDUCATION-
dc.identifier.pidcarachel07-
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COLLEGE OF ART AND PHYSICAL EDUCATION[S](예술·체육대학) > PHYSICAL EDUCATION(체육학과) > Articles
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