Autophagy Signaling in Skeletal Muscle of Infarcted Rats

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art_DOURADO_Autophagy_Signaling_in_Skeletal_Muscle_of_Infarcted_Rats_2014.PDF (4.25 MB)
Citações na Scopus
44
Tipo de produção
article
Data de publicação
2014
Editora
PUBLIC LIBRARY SCIENCE
DOI
Indexadores
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Autores
JANNIG, Paulo R.
MOREIRA, Jose B. N.
BECHARA, Luiz R. G.
BOZI, Luiz H. M.
BACURAU, Aline V.
MONTEIRO, Alex W. A.
WISLOFF, Ulrik
BRUM, Patricia C.
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
PLOS ONE, v.9, n.1, article ID e85820, 12p, 2014
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Heart failure (HF)-induced skeletal muscle atrophy is often associated to exercise intolerance and poor prognosis. Better understanding of the molecular mechanisms underlying HF-induced muscle atrophy may contribute to the development of pharmacological strategies to prevent or treat such condition. It has been shown that autophagy-lysosome system is an important mechanism for maintenance of muscle mass. However, its role in HF-induced myopathy has not been addressed yet. Therefore, the aim of the present study was to evaluate autophagy signaling in myocardial infarction (MI)-induced muscle atrophy in rats. Methods/Principal Findings: Wistar rats underwent MI or Sham surgeries, and after 12 weeks were submitted to echocardiography, exercise tolerance and histology evaluations. Cathepsin L activity and expression of autophagy-related genes and proteins were assessed in soleus and plantaris muscles by fluorimetric assay, qRT-PCR and immunoblotting, respectively. MI rats displayed exercise intolerance, left ventricular dysfunction and dilation, thereby suggesting the presence of HF. The key findings of the present study were: a) upregulation of autophagy-related genes (GABARAPL1, ATG7, BNIP3, CTSL1 and LAMP2) was observed only in plantaris while muscle atrophy was observed in both soleus and plantaris muscles, and b) Cathepsin L activity, Bnip3 and Fis1 protein levels, and levels of lipid hydroperoxides were increased specifically in plantaris muscle of MI rats. Conclusions: Altogether our results provide evidence for autophagy signaling regulation in HF-induced plantaris atrophy but not soleus atrophy. Therefore, autophagy-lysosome system is differentially regulated in atrophic muscles comprising different fiber-types and metabolic characteristics.
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URI
https://observatorio.fm.usp.br/handle/OPI/5502
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Coleções
Artigos e Materiais de Revistas Científicas - HC/InCor