Tlr4 participates in the responses of markers of apoptosis, inflammation, and ER stress to different acute exercise intensities in mice hearts

Autor(es):Mostrar menos -

de Vicente, Larissa G. ^[1] ; Pinto, Ana P. ^[1] ; Munoz, Vitor R. ^[2] ; Rovina, Rafael L. ^[3] ; da Rocha, Alisson L. ^[1] ; Gaspar, Rafael C. ^[2] ; da Silva, Lilian E. C. M. ^[4] ; Simabuco, Fernando M. ^[2] ; Frantz, Fabiani G. ^[5] ; Pauli, Jose R. ^[2] ; de Moura, Leandro P. ^[2] ; Cintra, Dennys E. ^[2] ; Ropelle, Eduardo R. ^[2] ; da Silva, Adelino S. R. ^{[3, 1]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Postgrad Program Rehabil & Funct Performance, BR-14040900 Ribeirao Preto, SP - Brazil

^[2] Univ Campinas UNICAMP, Sch Appl Sci, Lab Mol Biol Exercise LaBMEx, BR-13484350 Limeira, SP - Brazil

^[3] Univ Sao Paulo, Sch Phys Educ & Sport Ribeirao Preto, BR-14040900 Ribeirao Preto, SP - Brazil

^[4] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Ophthalmol Otorhinolaryngol & Head & Neck Su, BR-14040900 Ribeirao Preto - Brazil

^[5] Univ Sao Paulo, Dept Clin Toxicol & Bromatol Anal, Fac Pharmaceut Sci Ribeirao Preto, BR-14040900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Life Sciences; v. 240, JAN 1 2020.
• Citações Web of Science: 0

Resumo

Background: Toll-like receptor 4 (Tlr4) is recognized due to its role in the immune response. Also, this protein can participate in the signaling pathway of events triggered by physical exercise such as apoptosis, inflammation, and endoplasmic reticulum (ER) stress. The main objective of this study was to evaluate the role of Tlr4 in the markers of these events in the myocardium of mice submitted to acute physical exercise (APE) protocols at different intensities. Methods: Echocardiogram, RT-qPCR, and immunoblotting technique were used to evaluate the left ventricle of wild-type (WT) and Tlr4 knockout (Tlr4 KO) submitted to APE protocols at 45, 60, and 75% of their maximal velocity. Also, we performed the bioinformatics analysis to establish the connection of heart mRNA levels of Tlr4 with heart genes of inflammation and ER stress of several isogenic strains of BXD mice. Results: Under basal conditions, the Tlr4 deletion diminished the performance, and expression of inflammation and ER stress genes in the left ventricle, but increased the serum levels of CK, Il-17, and Tnf-alpha. Under the same exercise conditions, the Tlr4 deletion reduced the glycemia, serum levels of CK, Il-17, and Tnf-alpha, as well as genes and/or proteins related to apoptosis, inflammation and ER stress in the left ventricle, but increased the levels of CK-mb and LDH, as well as other genes related to apoptosis, inflammation, and ER stress in the left ventricle. Conclusion: Altogether, the current findings highlighted the effects of different acute exercise intensities were attenuated in the heart of Tlr4 KO mice. (AU)

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