Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , , , , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1111/acel.13467 http://hdl.handle.net/11449/222457 |
Resumo: | Protein quality control mechanisms decline during the process of cardiac aging. This enables the accumulation of protein aggregates and damaged organelles that contribute to age-associated cardiac dysfunction. Macroautophagy is the process by which post-mitotic cells such as cardiomyocytes clear defective proteins and organelles. We hypothesized that late-in-life exercise training improves autophagy, protein aggregate clearance, and function that is otherwise dysregulated in hearts from old vs. adult mice. As expected, 24-month-old male C57BL/6J mice (old) exhibited repressed autophagosome formation and protein aggregate accumulation in the heart, systolic and diastolic dysfunction, and reduced exercise capacity vs. 8-month-old (adult) mice (all p < 0.05). To investigate the influence of late-in-life exercise training, additional cohorts of 21-month-old mice did (old-ETR) or did not (old-SED) complete a 3-month progressive resistance treadmill running program. Body composition, exercise capacity, and soleus muscle citrate synthase activity improved in old-ETR vs. old-SED mice at 24 months (all p < 0.05). Importantly, protein expression of autophagy markers indicate trafficking of the autophagosome to the lysosome increased, protein aggregate clearance improved, and overall function was enhanced (all p < 0.05) in hearts from old-ETR vs. old-SED mice. These data provide the first evidence that a physiological intervention initiated late-in-life improves autophagic flux, protein aggregate clearance, and contractile performance in mouse hearts. |
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Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse heartsagingcardiac functionexerciseprotein aggregatesProtein quality control mechanisms decline during the process of cardiac aging. This enables the accumulation of protein aggregates and damaged organelles that contribute to age-associated cardiac dysfunction. Macroautophagy is the process by which post-mitotic cells such as cardiomyocytes clear defective proteins and organelles. We hypothesized that late-in-life exercise training improves autophagy, protein aggregate clearance, and function that is otherwise dysregulated in hearts from old vs. adult mice. As expected, 24-month-old male C57BL/6J mice (old) exhibited repressed autophagosome formation and protein aggregate accumulation in the heart, systolic and diastolic dysfunction, and reduced exercise capacity vs. 8-month-old (adult) mice (all p < 0.05). To investigate the influence of late-in-life exercise training, additional cohorts of 21-month-old mice did (old-ETR) or did not (old-SED) complete a 3-month progressive resistance treadmill running program. Body composition, exercise capacity, and soleus muscle citrate synthase activity improved in old-ETR vs. old-SED mice at 24 months (all p < 0.05). Importantly, protein expression of autophagy markers indicate trafficking of the autophagosome to the lysosome increased, protein aggregate clearance improved, and overall function was enhanced (all p < 0.05) in hearts from old-ETR vs. old-SED mice. These data provide the first evidence that a physiological intervention initiated late-in-life improves autophagic flux, protein aggregate clearance, and contractile performance in mouse hearts.Nutrition and Integrative Physiology University of UtahSchool of Dentistry Sao Paulo State UniversityMolecular Medicine Program University of UtahDivision of Cardiovascular Medicine and Pediatric Cardiology University of UtahGeorge E Wahlen VA Medical Center University of UtahSchool of Dentistry Sao Paulo State UniversityUniversity of UtahUniversidade Estadual Paulista (UNESP)Cho, Jae MinPark, Seul-KiGhosh, RajeshwaryLy, KellseyRamous, CarolineThompson, LaurenHansen, MicheleMattera, Maria Sara de Lima Coutinho [UNESP]Pires, Karla MariaFerhat, MarouaMookherjee, SohomWhitehead, Kevin J.Carter, KandisBuffolo, MárcioBoudina, SihemSymons, J. David2022-04-28T19:44:47Z2022-04-28T19:44:47Z2021-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1111/acel.13467Aging Cell.1474-97261474-9718http://hdl.handle.net/11449/22245710.1111/acel.134672-s2.0-85115298506Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengAging Cellinfo:eu-repo/semantics/openAccess2022-04-28T19:44:48Zoai:repositorio.unesp.br:11449/222457Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T14:27:01.095501Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts |
title |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts |
spellingShingle |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts Cho, Jae Min aging cardiac function exercise protein aggregates |
title_short |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts |
title_full |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts |
title_fullStr |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts |
title_full_unstemmed |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts |
title_sort |
Late-in-life treadmill training rejuvenates autophagy, protein aggregate clearance, and function in mouse hearts |
author |
Cho, Jae Min |
author_facet |
Cho, Jae Min Park, Seul-Ki Ghosh, Rajeshwary Ly, Kellsey Ramous, Caroline Thompson, Lauren Hansen, Michele Mattera, Maria Sara de Lima Coutinho [UNESP] Pires, Karla Maria Ferhat, Maroua Mookherjee, Sohom Whitehead, Kevin J. Carter, Kandis Buffolo, Márcio Boudina, Sihem Symons, J. David |
author_role |
author |
author2 |
Park, Seul-Ki Ghosh, Rajeshwary Ly, Kellsey Ramous, Caroline Thompson, Lauren Hansen, Michele Mattera, Maria Sara de Lima Coutinho [UNESP] Pires, Karla Maria Ferhat, Maroua Mookherjee, Sohom Whitehead, Kevin J. Carter, Kandis Buffolo, Márcio Boudina, Sihem Symons, J. David |
author2_role |
author author author author author author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
University of Utah Universidade Estadual Paulista (UNESP) |
dc.contributor.author.fl_str_mv |
Cho, Jae Min Park, Seul-Ki Ghosh, Rajeshwary Ly, Kellsey Ramous, Caroline Thompson, Lauren Hansen, Michele Mattera, Maria Sara de Lima Coutinho [UNESP] Pires, Karla Maria Ferhat, Maroua Mookherjee, Sohom Whitehead, Kevin J. Carter, Kandis Buffolo, Márcio Boudina, Sihem Symons, J. David |
dc.subject.por.fl_str_mv |
aging cardiac function exercise protein aggregates |
topic |
aging cardiac function exercise protein aggregates |
description |
Protein quality control mechanisms decline during the process of cardiac aging. This enables the accumulation of protein aggregates and damaged organelles that contribute to age-associated cardiac dysfunction. Macroautophagy is the process by which post-mitotic cells such as cardiomyocytes clear defective proteins and organelles. We hypothesized that late-in-life exercise training improves autophagy, protein aggregate clearance, and function that is otherwise dysregulated in hearts from old vs. adult mice. As expected, 24-month-old male C57BL/6J mice (old) exhibited repressed autophagosome formation and protein aggregate accumulation in the heart, systolic and diastolic dysfunction, and reduced exercise capacity vs. 8-month-old (adult) mice (all p < 0.05). To investigate the influence of late-in-life exercise training, additional cohorts of 21-month-old mice did (old-ETR) or did not (old-SED) complete a 3-month progressive resistance treadmill running program. Body composition, exercise capacity, and soleus muscle citrate synthase activity improved in old-ETR vs. old-SED mice at 24 months (all p < 0.05). Importantly, protein expression of autophagy markers indicate trafficking of the autophagosome to the lysosome increased, protein aggregate clearance improved, and overall function was enhanced (all p < 0.05) in hearts from old-ETR vs. old-SED mice. These data provide the first evidence that a physiological intervention initiated late-in-life improves autophagic flux, protein aggregate clearance, and contractile performance in mouse hearts. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-01-01 2022-04-28T19:44:47Z 2022-04-28T19:44:47Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1111/acel.13467 Aging Cell. 1474-9726 1474-9718 http://hdl.handle.net/11449/222457 10.1111/acel.13467 2-s2.0-85115298506 |
url |
http://dx.doi.org/10.1111/acel.13467 http://hdl.handle.net/11449/222457 |
identifier_str_mv |
Aging Cell. 1474-9726 1474-9718 10.1111/acel.13467 2-s2.0-85115298506 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Aging Cell |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1808128361586753536 |