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Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats

Cardiac endoplasmic reticulum (ER) stress through accumulation of misfolded proteins plays a pivotal role in cardiovascular diseases. In an attempt to reestablish ER homoeostasis, the unfolded protein response (UPR) is activated. However, if ER stress persists, sustained UPR activation leads to apop...

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Autores principales: Bozi, Luiz H. M., Jannig, Paulo R., Rolim, Natale, Voltarelli, Vanessa A., Dourado, Paulo M. M., Wisløff, Ulrik, Brum, Patricia C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082404/
https://www.ncbi.nlm.nih.gov/pubmed/27305869
http://dx.doi.org/10.1111/jcmm.12894
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author Bozi, Luiz H. M.
Jannig, Paulo R.
Rolim, Natale
Voltarelli, Vanessa A.
Dourado, Paulo M. M.
Wisløff, Ulrik
Brum, Patricia C.
author_facet Bozi, Luiz H. M.
Jannig, Paulo R.
Rolim, Natale
Voltarelli, Vanessa A.
Dourado, Paulo M. M.
Wisløff, Ulrik
Brum, Patricia C.
author_sort Bozi, Luiz H. M.
collection PubMed
description Cardiac endoplasmic reticulum (ER) stress through accumulation of misfolded proteins plays a pivotal role in cardiovascular diseases. In an attempt to reestablish ER homoeostasis, the unfolded protein response (UPR) is activated. However, if ER stress persists, sustained UPR activation leads to apoptosis. There is no available therapy for ER stress relief. Considering that aerobic exercise training (AET) attenuates oxidative stress, mitochondrial dysfunction and calcium imbalance, it may be a potential strategy to reestablish cardiac ER homoeostasis. We test the hypothesis that AET would attenuate impaired cardiac ER stress after myocardial infarction (MI). Wistar rats underwent to either MI or sham surgeries. Four weeks later, rats underwent to 8 weeks of moderate‐intensity AET. Myocardial infarction rats displayed cardiac dysfunction and lung oedema, suggesting heart failure. Cardiac dysfunction in MI rats was paralleled by increased protein levels of UPR markers (GRP78, DERLIN‐1 and CHOP), accumulation of misfolded and polyubiquitinated proteins, and reduced chymotrypsin‐like proteasome activity. These results suggest an impaired cardiac protein quality control. Aerobic exercise training improved exercise capacity and cardiac function of MI animals. Interestingly, AET blunted MI‐induced ER stress by reducing protein levels of UPR markers, and accumulation of both misfolded and polyubiquinated proteins, which was associated with restored proteasome activity. Taken together, our study provide evidence for AET attenuation of ER stress through the reestablishment of cardiac protein quality control, which contributes to better cardiac function in post‐MI heart failure rats. These results reinforce the importance of AET as primary non‐pharmacological therapy to cardiovascular disease.
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spelling pubmed-50824042016-11-01 Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats Bozi, Luiz H. M. Jannig, Paulo R. Rolim, Natale Voltarelli, Vanessa A. Dourado, Paulo M. M. Wisløff, Ulrik Brum, Patricia C. J Cell Mol Med Short Communication Cardiac endoplasmic reticulum (ER) stress through accumulation of misfolded proteins plays a pivotal role in cardiovascular diseases. In an attempt to reestablish ER homoeostasis, the unfolded protein response (UPR) is activated. However, if ER stress persists, sustained UPR activation leads to apoptosis. There is no available therapy for ER stress relief. Considering that aerobic exercise training (AET) attenuates oxidative stress, mitochondrial dysfunction and calcium imbalance, it may be a potential strategy to reestablish cardiac ER homoeostasis. We test the hypothesis that AET would attenuate impaired cardiac ER stress after myocardial infarction (MI). Wistar rats underwent to either MI or sham surgeries. Four weeks later, rats underwent to 8 weeks of moderate‐intensity AET. Myocardial infarction rats displayed cardiac dysfunction and lung oedema, suggesting heart failure. Cardiac dysfunction in MI rats was paralleled by increased protein levels of UPR markers (GRP78, DERLIN‐1 and CHOP), accumulation of misfolded and polyubiquitinated proteins, and reduced chymotrypsin‐like proteasome activity. These results suggest an impaired cardiac protein quality control. Aerobic exercise training improved exercise capacity and cardiac function of MI animals. Interestingly, AET blunted MI‐induced ER stress by reducing protein levels of UPR markers, and accumulation of both misfolded and polyubiquinated proteins, which was associated with restored proteasome activity. Taken together, our study provide evidence for AET attenuation of ER stress through the reestablishment of cardiac protein quality control, which contributes to better cardiac function in post‐MI heart failure rats. These results reinforce the importance of AET as primary non‐pharmacological therapy to cardiovascular disease. John Wiley and Sons Inc. 2016-06-16 2016-11 /pmc/articles/PMC5082404/ /pubmed/27305869 http://dx.doi.org/10.1111/jcmm.12894 Text en © 2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Short Communication
Bozi, Luiz H. M.
Jannig, Paulo R.
Rolim, Natale
Voltarelli, Vanessa A.
Dourado, Paulo M. M.
Wisløff, Ulrik
Brum, Patricia C.
Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats
title Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats
title_full Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats
title_fullStr Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats
title_full_unstemmed Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats
title_short Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats
title_sort aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082404/
https://www.ncbi.nlm.nih.gov/pubmed/27305869
http://dx.doi.org/10.1111/jcmm.12894
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