Aerobic exercise training rescues protein quality control disruption on white skeletal muscle induced by chronic kidney disease in rats

Aerobic exercise training rescues protein quality control disruption on white skeletal muscle induced by chronic kidney disease in rats

Author Almeida Monteiro De Moraes, Wilson Max Autor UNIFESP Google Scholar
Moraes de Souza, Pamella Ramona Google Scholar
da Paixao, Nathalie Alves Google Scholar
Oliveira de Sousa, Luis Gustavo Google Scholar
Ribeiro, Daniel Araki Autor UNIFESP Google Scholar
Marshall, Andrea G. Google Scholar
Prestes, Jonato Google Scholar
Irigoyen, Maria Claudia Google Scholar
Brum, Patricia Chakur Google Scholar
Medeiros, Alessandra Autor UNIFESP Google Scholar
Abstract We tested whether aerobic exercise training (AET) would modulate the skeletal muscle protein quality control (PQC) in a model of chronic kidney disease (CKD) in rats. Adult Wistar rats were evaluated in four groups: control (CS) or trained (CE), and 5/6 nephrectomy sedentary (5/6NxS) or trained (5/6NxE). Exercised rats were submitted to treadmill exercise (60min., five times/wk for 2months). We evaluated motor performance (tolerance to exercise on the treadmill and rotarod), cross-sectional area (CSA), gene and protein levels related to the unfolded protein response (UPR), protein synthesis/survive and apoptosis signalling, accumulated misfolded proteins, chymotrypsin-like proteasome activity (UPS activity), redox balance and heat-shock protein (HSP) levels in the tibialis anterior. 5/6NxS presented a trend towards to atrophy, with a reduction in motor performance, down-regulation of protein synthesis and up-regulation of apoptosis signalling

increases in UPS activity, misfolded proteins, GRP78, derlin, HSP27 and HSP70 protein levels, ATF4 and GRP78 genes

and increase in oxidative damage compared to CS group. In 5/6NxE, we observed a restoration in exercise tolerance, accumulated misfolded proteins, UPS activity, protein synthesis/apoptosis signalling, derlin, HSPs protein levels as well as increase in ATF4, GRP78 genes and ATF6 protein levels accompanied by a decrease in oxidative damage and increased catalase and glutathione peroxidase activities. The results suggest a disruption of PQC in white muscle fibres of CKD rats previous to the atrophy. AET can rescue this disruption for the UPR, prevent accumulated misfolded proteins and reduce oxidative damage, HSPs protein levels and exercise tolerance.
Keywords chronic kidney disease
aerobic exercise training
skeletal muscle
protein quality control
unfolded protein response
xmlui.dri2xhtml.METS-1.0.item-coverage Hoboken
Language English
Sponsor Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
Fundacao de Amparoa Pesquisa do Estado de Sao Paulo (FAPESP)
Grant number CAPES: 12/51090-1
FAPESP: 15/198936-0
Date 2018
Published in Journal Of Cellular And Molecular Medicine. Hoboken, v. 22, n. 3, p. 1452-1463, 2018.
ISSN 1582-4934 (Sherpa/Romeo, impact factor)
Publisher Wiley
Extent 1452-1463
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000426069300007

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