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

Autor: Luís G O de Sousa, Maria Claudia Irigoyen, Daniel Araki Ribeiro, Jonato Prestes, Andrea G. Marshall, Patricia Chakur Brum, Wilson Max Almeida Monteiro de Moraes, Alessandra Medeiros, N. A. Paixão, Pamella Ramona Moraes de Souza
Jazyk: angličtina
Rok vydání: 2017
Předmět:
0301 basic medicine
Male
030204 cardiovascular system & hematology
Kidney Function Tests
Nephrectomy
0302 clinical medicine
Heat-Shock Proteins
chemistry.chemical_classification
biology
Glutathione peroxidase
unfolded protein response
Catalase
Muscular Atrophy
medicine.anatomical_structure
Molecular Medicine
Original Article
Signal Transduction
medicine.medical_specialty
Proteasome Endopeptidase Complex
Motor Activity
03 medical and health sciences
Atrophy
Hsp27
Internal medicine
Physical Conditioning
Animal

medicine
Aerobic exercise
Animals
protein quality control
skeletal muscle
Rats
Wistar

Renal Insufficiency
Chronic

Muscle
Skeletal

Glutathione Peroxidase
business.industry
ATF4
Skeletal muscle
RATOS WISTAR
Cell Biology
Original Articles
medicine.disease
Activating Transcription Factor 4
Hsp70
Activating Transcription Factor 6
Rats
Disease Models
Animal

030104 developmental biology
Endocrinology
chemistry
Gene Expression Regulation
Protein Biosynthesis
Rotarod Performance Test
Unfolded protein response
biology.protein
aerobic exercise training
Sedentary Behavior
business
chronic kidney disease
Zdroj: Journal of Cellular and Molecular Medicine
Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
ISSN: 1582-4934
1582-1838
Popis: 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, 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 ATF6α 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.
Databáze: OpenAIRE