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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.)

Aerobic Exercise Training Induces the Mitonuclear Imbalance and UPRmt in the Skeletal Muscle of Aged Mice

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Author(s):
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Cordeiro, V, Andre ; Bricola, Rafael S. [1] ; Braga, Renata R. [1] ; Lenhare, Luciene [1] ; Silva, Vagner R. R. [1] ; Anaruma, Chadi P. [1, 2] ; Katashima, Carlos K. [1] ; Crisol, Barbara M. [1] ; Simabuco, Fernando M. [3] ; Silva, Adelino S. R. [4, 5] ; Cintra, Dennys E. [6] ; Moura, Leandro P. [1, 2, 7] ; Pauli, Jose R. [1, 7] ; Ropelle, Eduardo R. [1, 7, 8]
Total Authors: 14
Affiliation:
[1] Cordeiro, Andre, V, Univ Estadual Campinas, Lab Mol Biol Exercise, Limeira - Brazil
[2] Sao Paulo State Univ, Inst Biosci, Dept Phys Educ, Rio Claro - Brazil
[3] Univ Estadual Campinas, Lab Funct Properties Foods, Limeira - Brazil
[4] Univ Sao Paulo, Sch Phys Educ & Sport Ribeirao Preto, Ribeirao Preto - Brazil
[5] Univ Sao Paulo, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto - Brazil
[6] Univ Estadual Campinas, Lab Nutr Genom, Limeira - Brazil
[7] Univ Estadual Campinas, CEPECE Ctr Res Sport Sci, Sch Appl Sci, UNICAMP, Limeira - Brazil
[8] Univ Estadual Campinas, Fac Med Sci, Dept Internal Med, UNICAMP, Campinas, SP - Brazil
Total Affiliations: 8
Document type: Journal article
Source: JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES; v. 75, n. 12, p. 2258-2261, DEC 2020.
Web of Science Citations: 0
Abstract

The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial unfolded protein response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of aerobic exercise training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 months) and aged (24 months) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals. (AU)

FAPESP's process: 18/07634-9 - Evaluation of mitonuclear imbalance and UPRmt in the skeletal muscle of exercise mice: The role JNK and PKR.
Grantee:Eduardo Rochete Ropelle
Support Opportunities: Regular Research Grants