Autophagy signaling in hypertrophied muscles of diabetic and control rats

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Scervino, Maria V. M. ; Fortes, Marco A. S. ; Vitzel, Kaio F. ; de Souza, Diego R. ; Murata, Gilson M. ; Santana, Giovanna O. ; da Silva, Eliane B. ; Levada-Pires, Adriana C. ; Kuwabara, Wilson M. T. ; Loureiro, Tatiana C. A. ; Curi, Rui

• Tipo de documento: Artigo Científico
• Fonte: FEBS OPEN BIO; v. 13, n. 9, p. 14-pg., 2023-07-26.

Resumo

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. (AU)

• Processo FAPESP: 16/11661-6 - Envolvimento da autofagia na hipertrofia do músculo esquelético em ratos com diabetes mellitus tipo-1
• Beneficiário: Maria Vitoria Martins Scervino
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 16/15766-7 - Hipertrofia do músculo esquelético em ratos com diabetes mellitus tipo I
• Beneficiário: Rui Curi
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 19/19097-0 - Envolvimento da inflamação na resposta hipertrófica do músculo esquelético em ratos com Diabetes Mellitus Tipo I
• Beneficiário: Maria Vitoria Martins Scervino
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto
• Processo FAPESP: 20/00707-0 - Envolvimento da inflamação na hipertrofia do músculo esquelético e performance no exercício físico
• Beneficiário: Rui Curi
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 19/02175-9 - Avaliação das vias de síntese e degradação de proteínas na resposta hipertrófica dos músculos EDL e sóleo em ratos Goto Kakizaki
• Beneficiário: Giovanna de Oliveira Santana
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica