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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Exercise prevents impaired autophagy and proteostasis in a model of neurogenic myopathy

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Autor(es):
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Campos, Juliane C. [1] ; Baehr, Leslie M. [2] ; Gomes, Katia M. S. [1] ; Bechara, Luiz R. G. [1] ; Voltarelli, Vanessa A. [3] ; Bozi, Luiz H. M. [1] ; Ribeiro, Marcio A. C. [1] ; Ferreira, Nikolas D. [1] ; Moreira, Jose B. N. [3, 4] ; Brum, Patricia C. [3] ; Bodine, Sue C. [2] ; Ferreira, Julio C. B. [1]
Número total de Autores: 12
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, BR-05508000 Sao Paulo - Brazil
[2] Univ Iowa, Endocrinol & Metab Div, Dept Internal Med, Iowa City, IA 52242 - USA
[3] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508030 Sao Paulo - Brazil
[4] Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Cardiac Exercise Res Grp, N-7006 Trondheim - Norway
Número total de Afiliações: 4
Tipo de documento: Artigo Científico
Fonte: SCIENTIFIC REPORTS; v. 8, AUG 7 2018.
Citações Web of Science: 3
Resumo

Increased proteolytic activity has been widely associated with skeletal muscle atrophy. However, elevated proteolysis is also critical for the maintenance of cellular homeostasis by disposing cytotoxic proteins and non-functioning organelles. We recently demonstrated that exercise activates autophagy and re-establishes proteostasis in cardiac diseases. Here, we characterized the impact of exercise on skeletal muscle autophagy and proteostasis in a model of neurogenic myopathy induced by sciatic nerve constriction in rats. Neurogenic myopathy, characterized by progressive atrophy and impaired contractility, was paralleled by accumulation of autophagy-related markers and loss of acute responsiveness to both colchicine and chloroquine. These changes were correlated with elevated levels of damaged proteins, chaperones and pro-apoptotic markers compared to control animals. Sustained autophagy inhibition using chloroquine in rats (50 mg. kg(-1). day(-1)) or muscle-specific deletion of Atg7 in mice was sufficient to impair muscle contractility in control but not in neurogenic myopathy, suggesting that dysfunctional autophagy is critical in skeletal muscle pathophysiology. Finally, 4 weeks of aerobic exercise training (moderate treadmill running, 5x/week, 1 h/day) prior to neurogenic myopathy improved skeletal muscle autophagic flux and proteostasis. These changes were followed by spared muscle mass and better contractility properties. Taken together, our findings suggest the potential value of exercise in maintaining skeletal muscle proteostasis and slowing down the progression of neurogenic myopathy. (AU)

Processo FAPESP: 12/14416-1 - Controle de qualidade de proteína na disfunção/atrofia muscular esquelética: papel do receptor beta2- adrenérgico
Beneficiário:Juliane Cruz Campos
Linha de fomento: Bolsas no Brasil - Doutorado
Processo FAPESP: 15/22814-5 - Câncer e coração: novos paradigmas de diagnóstico e tratamento
Beneficiário:Carlos Eduardo Negrão
Linha de fomento: Auxílio à Pesquisa - Temático
Processo FAPESP: 15/20783-5 - Controle de qualidade de proteína na disfunção/atrofia muscular esquelética: papel do receptor 22- adrenérgico
Beneficiário:Julio Cesar Batista Ferreira
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 16/01633-5 - Papel protetor da estimulação Beta2-adrenérgica na disfunção/atrofia muscular esquelética: contribuição do sistema lisossomal-autofágico
Beneficiário:Juliane Cruz Campos
Linha de fomento: Bolsas no Exterior - Estágio de Pesquisa - Doutorado