Autophagy signaling in hypertrophied muscles of diabetic and control rats

Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic ra...

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Main Authors: Maria V. M. Scervino, Marco A. S. Fortes, Kaio F. Vitzel, Diego R. deSouza, Gilson M. Murata, Giovanna O. Santana, Eliane B. daSilva, Adriana C. Levada‐Pires, Wilson M. T. Kuwabara, Tatiana C. A. Loureiro, Rui Curi
Format: Article
Language:English
Published: Wiley 2023-09-01
Series:FEBS Open Bio
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Online Access:https://doi.org/10.1002/2211-5463.13677
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author Maria V. M. Scervino
Marco A. S. Fortes
Kaio F. Vitzel
Diego R. deSouza
Gilson M. Murata
Giovanna O. Santana
Eliane B. daSilva
Adriana C. Levada‐Pires
Wilson M. T. Kuwabara
Tatiana C. A. Loureiro
Rui Curi
author_facet Maria V. M. Scervino
Marco A. S. Fortes
Kaio F. Vitzel
Diego R. deSouza
Gilson M. Murata
Giovanna O. Santana
Eliane B. daSilva
Adriana C. Levada‐Pires
Wilson M. T. Kuwabara
Tatiana C. A. Loureiro
Rui Curi
author_sort Maria V. M. Scervino
collection DOAJ
description Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3‐day streptozotocin‐induced diabetic rats, an experimental model for type 1 diabetes mellitus (T1DM). EDL muscles showed increased levels of basal autophagy signaling proteins. The diabetic state did not affect the extent of overload‐induced hypertrophy or the levels of autophagy signaling proteins (p‐ULK1, Beclin‐1, Atg5, Atg12‐5, Atg7, Atg3, LC3‐I and II, and p62) in either muscle. The p‐ULK‐1, Beclin‐1, and p62 protein expression levels were higher in the EDL muscle than in the soleus before the hypertrophic stimulus. On the contrary, the soleus muscle exhibited increased autophagic signaling after overload‐induced hypertrophy, with increases in Beclin‐1, Atg5, Atg12‐5, Atg7, Atg3, and LC3‐I expression in the control and diabetic groups, in addition to p‐ULK‐1 in the control groups. After hypertrophy, Beclin‐1 and Atg5 levels increased in the EDL muscle of both groups, while p‐ULK1 and LC3‐I increased in the control group. In conclusion, the baseline EDL muscle exhibited higher autophagy than the soleus muscle. Although TDM1 promotes skeletal muscle mass loss and strength reduction, it did not significantly alter the extent of overload‐induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.
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spelling doaj.art-952bb9807c304abfa7ef68e5adfc3bc02023-09-04T13:56:57ZengWileyFEBS Open Bio2211-54632023-09-011391709172210.1002/2211-5463.13677Autophagy signaling in hypertrophied muscles of diabetic and control ratsMaria V. M. Scervino0Marco A. S. Fortes1Kaio F. Vitzel2Diego R. deSouza3Gilson M. Murata4Giovanna O. Santana5Eliane B. daSilva6Adriana C. Levada‐Pires7Wilson M. T. Kuwabara8Tatiana C. A. Loureiro9Rui Curi10Instituto de Ciências da Atividade Física e Esporte (ICAFE) Universidade Cruzeiro do Sul São Paulo BrazilDepartmento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas Universidade de São Paulo BrazilSchool of Health Sciences, College of Health Massey University Auckland New ZealandInstituto de Ciências da Atividade Física e Esporte (ICAFE) Universidade Cruzeiro do Sul São Paulo BrazilDepartmento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas Universidade de São Paulo BrazilInstituto de Ciências da Atividade Física e Esporte (ICAFE) Universidade Cruzeiro do Sul São Paulo BrazilInstituto de Ciências da Atividade Física e Esporte (ICAFE) Universidade Cruzeiro do Sul São Paulo BrazilInstituto de Ciências da Atividade Física e Esporte (ICAFE) Universidade Cruzeiro do Sul São Paulo BrazilDepartmento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas Universidade de São Paulo BrazilDepartmento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas Universidade de São Paulo BrazilInstituto de Ciências da Atividade Física e Esporte (ICAFE) Universidade Cruzeiro do Sul São Paulo BrazilAutophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3‐day streptozotocin‐induced diabetic rats, an experimental model for type 1 diabetes mellitus (T1DM). EDL muscles showed increased levels of basal autophagy signaling proteins. The diabetic state did not affect the extent of overload‐induced hypertrophy or the levels of autophagy signaling proteins (p‐ULK1, Beclin‐1, Atg5, Atg12‐5, Atg7, Atg3, LC3‐I and II, and p62) in either muscle. The p‐ULK‐1, Beclin‐1, and p62 protein expression levels were higher in the EDL muscle than in the soleus before the hypertrophic stimulus. On the contrary, the soleus muscle exhibited increased autophagic signaling after overload‐induced hypertrophy, with increases in Beclin‐1, Atg5, Atg12‐5, Atg7, Atg3, and LC3‐I expression in the control and diabetic groups, in addition to p‐ULK‐1 in the control groups. After hypertrophy, Beclin‐1 and Atg5 levels increased in the EDL muscle of both groups, while p‐ULK1 and LC3‐I increased in the control group. In conclusion, the baseline EDL muscle exhibited higher autophagy than the soleus muscle. Although TDM1 promotes skeletal muscle mass loss and strength reduction, it did not significantly alter the extent of overload‐induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.https://doi.org/10.1002/2211-5463.13677autolysosomeautophagosomeautophagy‐related geneshyperglycemiaprotein degradation
spellingShingle Maria V. M. Scervino
Marco A. S. Fortes
Kaio F. Vitzel
Diego R. deSouza
Gilson M. Murata
Giovanna O. Santana
Eliane B. daSilva
Adriana C. Levada‐Pires
Wilson M. T. Kuwabara
Tatiana C. A. Loureiro
Rui Curi
Autophagy signaling in hypertrophied muscles of diabetic and control rats
FEBS Open Bio
autolysosome
autophagosome
autophagy‐related genes
hyperglycemia
protein degradation
title Autophagy signaling in hypertrophied muscles of diabetic and control rats
title_full Autophagy signaling in hypertrophied muscles of diabetic and control rats
title_fullStr Autophagy signaling in hypertrophied muscles of diabetic and control rats
title_full_unstemmed Autophagy signaling in hypertrophied muscles of diabetic and control rats
title_short Autophagy signaling in hypertrophied muscles of diabetic and control rats
title_sort autophagy signaling in hypertrophied muscles of diabetic and control rats
topic autolysosome
autophagosome
autophagy‐related genes
hyperglycemia
protein degradation
url https://doi.org/10.1002/2211-5463.13677
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