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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Morphological and molecular aspects of immobilization-induced muscle atrophy in rats at different stages of postnatal development: the role of autophagy

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Author(s):
Foresto, Camila Silva ; Paula-Gomes, Silvia ; Silveira, Wilian Assis ; Graca, Flavia Aparecida ; Kettelhut, Isis do Carmo ; Pinheiro Goncalves, Dawit Albieiro ; Mattiello-Sverzut, Ana Claudia
Total Authors: 7
Document type: Journal article
Source: Journal of Applied Physiology; v. 121, n. 3, p. 646-660, SEP 1 2016.
Web of Science Citations: 3
Abstract

Muscle loss occurs following injury and immobilization in adulthood and childhood, which impairs the rehabilitation process; however, far fewer studies have been conducted analyzing atrophic response in infants. This work investigated first the morphological and molecular mechanisms involved in immobilization-induced atrophy in soleus muscles from rats at different stages of postnatal development {[}i.e., weanling (WR) and adult (AR) rats] and, second, the role of autophagy in regulating muscle plasticity during immobilization. Hindlimb immobilization for 10 days reduced muscle mass and fiber cross-sectional area, with more pronounced atrophy in WR, and induced slow-to-fast fiber switching. These effects were accompanied by a decrease in markers of protein synthesis and an increase in autophagy. The ubiquitin (Ub)-ligase MuRF1 and the ubiquitinated proteins were upregulated by immobilization in AR while the autolyzed form of mu-calpain was increased in WR. To further explore the role of autophagy in muscle abnormalities, AR were concomitantly immobilized and treated with colchicine, which blocks autophagosome-lysosome fusion. Colchicine-treated immobilized muscles had exacerbated atrophy and presented degenerative features. Despite Igf1/Akt signaling was downregulated in immobilized muscles from both age groups, Foxo1 and 4 phosphorylation was increased in WR. In the same group of animals, Foxo1 acetylation and Foxo1 and 4 content was increased and decreased, respectively. Our data show that muscle disorders induced by 10-day-immobilization occur in both age-dependent and -independent manners, an understanding that may optimize treatment outcomes in infants. We also provide further evidence that the strong inhibition of autophagy may be ineffective for treating muscle atrophy. (AU)

FAPESP's process: 13/08553-9 - The role of the beta-arrestin signaling pathway in the control of cardiac muscle mass and cardiomyocytes culture of rodents
Grantee:Sílvia de Paula Gomes
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 12/18861-0 - FOXO hyperacetylation as a mechanism of suppression of atrophy gene program induced by beta2-adrenergic signaling in rodent skeletal muscle
Grantee:Dawit Albieiro Pinheiro Gonçalves
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 12/24524-6 - Control of muscle mass by cAMP signaling pathway
Grantee:Isis Do Carmo Kettelhut
Support type: Research Projects - Thematic Grants
FAPESP's process: 10/11015-0 - Intracellular mechanisms involved in anticatabolic effect of the epinephrine in skeletal muscle of fasted rats
Grantee:Flávia Aparecida Graça
Support type: Scholarships in Brazil - Doctorate