Format

Send to

Choose Destination

See 1 citation found using an alternative search:

PLoS One. 2014 Jan 10;9(1):e85820. doi: 10.1371/journal.pone.0085820. eCollection 2014.

Autophagy signaling in skeletal muscle of infarcted rats.

Author information

1
Experimental Physiopathology - Medical School, University of Sao Paulo, Sao Paulo, Brazil ; School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil.
2
School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil ; K. G. Jensen Center of Exercise in Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
3
School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil.
4
Heart Institute - Medical School, University of Sao Paulo, Sao Paulo, Brazil.
5
K. G. Jensen Center of Exercise in Medicine, Norwegian University of Science and Technology, Trondheim, Norway.

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.

PMID:
24427319
PMCID:
PMC3888434
DOI:
10.1371/journal.pone.0085820
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center