Open AccessAerobic exercise training rescues protein quality control disruption on white skeletal muscle induced by chronic kidney disease in rats
Author(s) -
De Moraes Wilson Max Almeida Monteiro,
Souza Pamella Ramona Moraes,
Paixão Nathalie Alves,
Sousa Luís Gustavo Oliveira,
Ribeiro Daniel Araki,
Marshall Andrea G.,
Prestes Jonato,
Irigoyen Maria Claudia,
Brum Patricia Chakur,
Medeiros Alessandra
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13374
Subject(s) - skeletal muscle , muscle atrophy , heat shock protein , medicine , endocrinology , oxidative stress , apoptosis , chemistry , biology , biochemistry , gene
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 (60 min., five times/wk for 2 months). 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, GRP 78, derlin, HSP 27 and HSP 70 protein levels, ATF 4 and GRP 78 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, HSP s protein levels as well as increase in ATF 4, GRP 78 genes and ATF 6α 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, HSP s protein levels and exercise tolerance.