Augmented mitochondrial apoptotic signaling impairs C2C12 myoblast differentiation following cellular aging through sequential passaging

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MetadadosDescriçãoIdioma
Autor(es): dc.contributorUniversity of Waterloo-
Autor(es): dc.contributorUniversidade Estadual Paulista (UNESP)-
Autor(es): dc.creatorRahman, Fasih A.-
Autor(es): dc.creatorHian-Cheong, Dylan J.-
Autor(es): dc.creatorBoonstra, Kristen-
Autor(es): dc.creatorMa, Andrew-
Autor(es): dc.creatorThoms, James P.-
Autor(es): dc.creatorZago, Anderson S.-
Autor(es): dc.creatorQuadrilatero, Joe-
Data de aceite: dc.date.accessioned2025-08-21T15:15:55Z-
Data de disponibilização: dc.date.available2025-08-21T15:15:55Z-
Data de envio: dc.date.issued2025-04-29-
Data de envio: dc.date.issued2024-10-31-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.1002/jcp.31155-
Fonte completa do material: dc.identifierhttps://hdl.handle.net/11449/304071-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/304071-
Descrição: dc.descriptionAging is associated with the steady decline of several cellular processes. The loss of skeletal muscle mass, termed sarcopenia, is one of the major hallmarks of aging. Aged skeletal muscle exhibits a robust reduction in its regenerative capacity due to dysfunction (i.e., senescence, lack of self-renewal, and impaired differentiation) of resident muscle stem cells, called satellite cells. To replicate aging in vitro, immortalized skeletal muscle cells (myoblasts) can be treated with various agents to mimic age-related dysfunction; however, these come with their own set of limitations. In the present study, we used sequential passaging of mouse myoblasts to mimic impaired differentiation that is observed in aged skeletal muscle. Further, we investigated mitochondrial apoptotic mechanisms to better understand the impaired differentiation in these “aged” cells. Our data shows that sequential passaging (>20 passages) of myoblasts is accompanied with significant reductions in differentiation and elevated cell death. Furthermore, high-passage (HP) myoblasts exhibit greater mitochondrial-mediated apoptotic signaling through mitochondrial BAX translocation, CYCS and AIFM1 release, and caspase-9 activation. Finally, we show that inhibition of mitochondrial outer membrane permeability partly recovered differentiation in HP myoblasts. Together, our findings suggests that mitochondrial apoptotic signaling is a contributing factor to the diminished differentiation that is observed in aged myoblasts.-
Descrição: dc.descriptionNatural Sciences and Engineering Research Council of Canada-
Descrição: dc.descriptionDepartment of Kinesiology and Health Sciences University of Waterloo-
Descrição: dc.descriptionDepartment of Physical Education School of Sciences Sao Paulo State University-
Descrição: dc.descriptionDepartment of Physical Education School of Sciences Sao Paulo State University-
Idioma: dc.languageen-
Relação: dc.relationJournal of Cellular Physiology-
???dc.source???: dc.sourceScopus-
Palavras-chave: dc.subjectaging-
Palavras-chave: dc.subjectapoptotic signaling-
Palavras-chave: dc.subjectdifferentiation-
Palavras-chave: dc.subjecthigh-passage-
Palavras-chave: dc.subjectmitochondria-
Palavras-chave: dc.subjectskeletal muscle-
Título: dc.titleAugmented mitochondrial apoptotic signaling impairs C2C12 myoblast differentiation following cellular aging through sequential passaging-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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