Advanced search
Start date
Betweenand
Related content
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Autophagy Signaling in Skeletal Muscle of Infarcted Rats

Full text
Author(s):
Jannig, Paulo R. [1, 2] ; Moreira, Jose B. N. [1, 3] ; Bechara, Luiz R. G. [1] ; Bozi, Luiz H. M. [1] ; Bacurau, Aline V. [1] ; Monteiro, Alex W. A. [1] ; Dourado, Paulo M. [4] ; Wisloff, Ulrik [3] ; Brum, Patricia C. [1, 2]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, Sch Phys Educ & Sport, Sao Paulo - Brazil
[2] Univ Sao Paulo, Expt Physiopathol Med Sch, Sao Paulo - Brazil
[3] Norwegian Univ Sci & Technol, KG Jensen Ctr Exercise Med, N-7034 Trondheim - Norway
[4] Univ Sao Paulo, Sch Med, Inst Heart, Sao Paulo - Brazil
Total Affiliations: 4
Document type: Journal article
Source: PLoS One; v. 9, n. 1 JAN 10 2014.
Web of Science Citations: 31
Abstract

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. (AU)

FAPESP's process: 10/14567-4 - Role of the lysosomal/autophagic proteolytic system in skeletal muscle of animals with heart failure
Grantee:Paulo Roberto Jannig
Support type: Scholarships in Brazil - Master
FAPESP's process: 10/50048-1 - Cellular and functional bases of exercise in cardiovascular diseases
Grantee:Carlos Eduardo Negrão
Support type: Research Projects - Thematic Grants