Pós-Graduação e seus processos / Science processes
Autor: Frederico Gerlinger | Publicado: 2016-12-28T13:55:00-02:00


Nesses últimos meses tenho focado nos esforços das
minhas publicações/estudos que estavam pendentes, dentre esses estava o meu
trabalho de pós-doutorado que terminei no início de 2015. E nessa última semana
tive a confirmação da publicação desse artigo. Curiosamente obtive essa informação
da publicação enquanto realizava um curso sobre divulgação cientifica, que
discutia a importância da divulgação da ciência produzida nas universidades
para a sociedade. E parte desse processo da divulgação e tornar o conhecimento
produzido em projetos de pesquisa em publicações na forma de artigo. Esse
estudo teve como cerne investigar mecanismos de proteólise muscular, ou seja,
perda de massas muscular, em animais diabéticos.





http://link.springer.com/article/10.1007%2Fs11010-016-2910-z








Over the last few months I’ve had focused in my manuscripts and one of them was my postdoctoral's study that I finished in 2015. Last week I received the accept email of this article. I'm so proud and glad about this article accepted.




Mol Cell Biochem.&nbsp;2016 Dec 20. doi: 10.1007/s11010-016-2910-z. [Epub ahead of print]

Dysregulation between TRIM63/FBXO32 expression and soleus muscle wasting in diabetic rats: potential role of miR-1-3p, -29a/b-3p, and -133a/b-3p.

Gerlinger-Romero&nbsp;F1,&nbsp;Yonamine CY2,&nbsp;Junior DC2,&nbsp;Esteves JV2,&nbsp;Machado UF2.


Author information





Abstract



Diabetes mellitus (DM) induces a variable degree of muscle sarcopenia, which may be related to protein degradation and to the expression of both E3 ubiquitin ligases and some specific microRNAs (miRNAs). The present study investigated the effect of diabetes and acute muscle contraction upon the TRIM63 and FBXO32 expression as well as the potential involvement of some miRNAs. Diabetes was induced by streptozotocin and studied after 30&nbsp;days. Soleus muscles were harvested, stimulated to contract in vitro for twitch tension analysis (0.5&nbsp;Hz), 30&nbsp;min later for tetanic analysis (100&nbsp;Hz), and 30&nbsp;min later were frozen. TRIM63 and FBXO32 proteins were quantified by western blotting; Trim63 mRNA, Fbxo32 mRNA, miR-1-3p, miR-29a-3p, miR-29b-3p, miR-133a-3p, and miR-133b-3p were quantified by qPCR. Diabetes induced sarcopenia by decreasing (P&nbsp;&lt;&nbsp;0.05) muscle weight/tibia length index, maximum tetanic contraction and relaxation rates, and absolute twitch and tetanic forces (P&nbsp;&lt;&nbsp;0.05). Diabetes decreased (P&nbsp;&lt;&nbsp;0.05) the Trim63 and Fbxo32 mRNAs (30%) and respective proteins (60%), and increased (P&nbsp;&lt;&nbsp;0.01) the miR-29b-3p (2.5-fold). In muscle from diabetic rats, acute contractile stimulus increased TRIM63 protein, miR-1-3p, miR-29a-3p, and miR-133a/b-3p, but decreased miR-29b-3p (P&nbsp;&lt;&nbsp;0.05). Independent of the metabolic condition, after muscle contraction, both TRIM63 and FBXO32 proteins correlated significantly with miR-1-3p, miR-29a/b-3p, and miR-133a/b-3p. All diabetes-induced regulations were reversed by insulin treatment. Concluding, the results depict that muscle wasting in long-term insulinopenic condition may not be accompanied by increased proteolysis, pointing out the protein synthesis as an important modulator of muscle sarcopenia in DM.





KEYWORDS:

Acute contraction; Atrogene; Sarcopenia; Soleus; Streptozotocin