IL-6 deletion decreased REV-ERBα protein and influenced autophagy and mitochondrial markers in the skeletal muscle after acute exercise

Registro completo de metadados
MetadadosDescriçãoIdioma
Autor(es): dc.contributorUniversidade de São Paulo (USP)-
Autor(es): dc.contributorUniversidade Estadual de Campinas (UNICAMP)-
Autor(es): dc.contributorUniversidade Estadual Paulista (UNESP)-
Autor(es): dc.creatorPinto, Ana P.-
Autor(es): dc.creatorMuñoz, Vitor R.-
Autor(es): dc.creatorda Rocha, Alisson L.-
Autor(es): dc.creatorRovina, Rafael L.-
Autor(es): dc.creatorFerrari, Gustavo D.-
Autor(es): dc.creatorAlberici, Luciane C.-
Autor(es): dc.creatorSimabuco, Fernando M.-
Autor(es): dc.creatorTeixeira, Giovana R.-
Autor(es): dc.creatorPauli, José R.-
Autor(es): dc.creatorde Moura, Leandro P.-
Autor(es): dc.creatorCintra, Dennys E.-
Autor(es): dc.creatorRopelle, Eduardo R.-
Autor(es): dc.creatorFreitas, Ellen C.-
Autor(es): dc.creatorRivas, Donato A.-
Autor(es): dc.creatorda Silva, Adelino S. R.-
Data de aceite: dc.date.accessioned2025-08-21T15:54:37Z-
Data de disponibilização: dc.date.available2025-08-21T15:54:37Z-
Data de envio: dc.date.issued2023-07-29-
Data de envio: dc.date.issued2023-07-29-
Data de envio: dc.date.issued2022-10-13-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.3389/fimmu.2022.953272-
Fonte completa do material: dc.identifierhttp://hdl.handle.net/11449/247822-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/247822-
Descrição: dc.descriptionInterleukin 6 (IL-6) acts as a pro and anti-inflammatory cytokine, has an intense correlation with exercise intensity, and activates various pathways such as autophagy and mitochondrial unfolded protein response. Also, IL-6 is interconnected to circadian clock-related inflammation and can be suppressed by the nuclear receptor subfamily 1, group D, member 1 (Nr1d1, protein product REV-ERBα). Since IL-6 is linked to physical exercise-modulated metabolic pathways such as autophagy and mitochondrial metabolism, we investigated the relationship of IL-6 with REV-ERBα in the adaptations of these molecular pathways in response to acute intense physical exercise in skeletal muscle. The present study was divided into three experiments. In the first one, wild-type (WT) and IL-6 knockout (IL-6 KO) mice were divided into three groups: Basal time (Basal; sacrificed before the acute exercise), 1 hour (1hr post-Ex; sacrificed 1 hour after the acute exercise), and 3 hours (3hr post-Ex; sacrificed 3 hours after the acute exercise). In the second experiment, C2C12 cells received IL-6 physiological concentrations or REV-ERBα agonist, SR9009. In the last experiment, WT mice received SR9009 injections. After the protocols, the gastrocnemius muscle or the cells were collected for reverse transcription-quantitative polymerase chain reaction (RTq-PCR) and immunoblotting techniques. In summary, the downregulation of REV-ERBα, autophagic flux, and most mitochondrial genes was verified in the IL-6 KO mice independent of exercise. The WT and IL-6 KO treated with SR9009 showed an upregulation of autophagic genes. C2C12 cells receiving IL-6 did not modulate the Nr1d1 mRNA levels but upregulated the expression of some mitochondrial genes. However, when treated with SR9009, IL-6 and mitochondrial gene expression were upregulated in C2C12 cells. The autophagic flux in C2C12 suggest the participation of REV-ERBα protein in the IL-6-induced autophagy. In conclusion, the present study verified that the adaptations required through physical exercise (increases in mitochondrial content and improvement of autophagy machinery) might be intermediated by an interaction between IL-6 and REVERBα.-
Descrição: dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)-
Descrição: dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
Descrição: dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
Descrição: dc.descriptionSchool of Physical Education and Sport of Ribeirão Preto University of São Paulo (USP)-
Descrição: dc.descriptionPostgraduate Program in Rehabilitation and Functional Performance Ribeirão Preto Medical School University of São Paulo (USP)-
Descrição: dc.descriptionDepartment of Biomolecular Sciences School of Pharmaceutical Sciences of Ribeirao Preto Faculty of Pharmaceutical Sciences of Ribeirao Preto University of São Paulo (FCFRP USP)-
Descrição: dc.descriptionLaboratory of Molecular Biology of Exercise (LaBMEx) School of Applied Sciences University of Campinas (UNICAMP)-
Descrição: dc.descriptionDepartment of Biochemistry Federal University of São Paulo (UNIFESP)-
Descrição: dc.descriptionMulticentric Program of Postgraduate in Physiological Sciences School of Dentistry of Araçatuba São Paulo State University (UNESP)-
Descrição: dc.descriptionDepartment of Physical Education State University of São Paulo (UNESP)-
Descrição: dc.descriptionMulticentric Program of Postgraduate in Physiological Sciences School of Dentistry of Araçatuba São Paulo State University (UNESP)-
Descrição: dc.descriptionDepartment of Physical Education State University of São Paulo (UNESP)-
Descrição: dc.descriptionFAPESP: 2017/12765-2-
Descrição: dc.descriptionFAPESP: 2018/14818-9-
Descrição: dc.descriptionFAPESP: 2019/11820-5-
Descrição: dc.descriptionFAPESP: 2019/21709-4-
Descrição: dc.descriptionFAPESP: 2020/13443-1-
Descrição: dc.descriptionFAPESP: 2021/08692-5-
Descrição: dc.descriptionFAPESP: 2021/08693-1-
Idioma: dc.languageen-
Relação: dc.relationFrontiers in Immunology-
???dc.source???: dc.sourceScopus-
Palavras-chave: dc.subjectautophagic flux-
Palavras-chave: dc.subjectC2C12 cells-
Palavras-chave: dc.subjectgenetic deletion-
Palavras-chave: dc.subjectmitochondria-
Palavras-chave: dc.subjectNr1d1-
Palavras-chave: dc.subjectpharmacological treatment-
Título: dc.titleIL-6 deletion decreased REV-ERBα protein and influenced autophagy and mitochondrial markers in the skeletal muscle after acute exercise-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

Não existem arquivos associados a este item.