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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

TLR4 deletion increases basal energy expenditure and attenuates heart apoptosis and ER stress but mitigates the training-induced cardiac function and performance improvement

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Author(s):
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de Vicente, Larissa G. [1] ; Munoz, Vitor R. [2] ; Pinto, Ana P. [1] ; Rovina, Rafael L. [3] ; da Rocha, Alisson L. [1] ; Marafon, Bruno B. [3] ; de A Tavares, Maria Eduarda [4] ; Teixeira, Giovana R. [5, 4] ; Ferrari, Gustavo D. [6] ; Alberici, Luciane C. [6] ; Frantz, Fabiani G. [7] ; Simabuco, Fernando M. [2] ; Ropelle, Eduardo R. [2] ; de Moura, Leandro P. [2] ; Cintra, Dennys E. [2] ; Pauli, Jose R. [2] ; da Silva, Adelino S. R. [3, 1]
Total Authors: 17
Affiliation:
[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto, SP - Brazil
[2] Univ Estadual Campinas, UNICAMP, Sch Appl Sci, Lab Mol Biol Exercise LaBMEx, Limeira, SP - Brazil
[3] Univ Sao Paulo, Sch Phys Educ & Sport Ribeirao Preto, Ribeirao Preto, SP - Brazil
[4] Sao Paulo State Univ, UNESP, Multictr Grad Program Physiol Sci, SBFis, Aracatuba, SP - Brazil
[5] State Univ Sao Paulo, UNESP, Dept Phys Educ, Presidente Prudente, SP - Brazil
[6] Univ Sao Paulo, FCFRP USP, Sch Pharmaceut Sci Ribeirao Preto, Dept Biomol Sci, Ribeirao Preto, SP - Brazil
[7] Univ Sao Paulo, Sch Pharmaceut Sci Ribeirao Preto, Dept Clin Toxicol & Bromatol Anal, Ribeirao Preto, SP - Brazil
Total Affiliations: 7
Document type: Journal article
Source: Life Sciences; v. 285, NOV 15 2021.
Web of Science Citations: 0
Abstract

Strategies capable of attenuating TLR4 can attenuate metabolic processes such as inflammation, endoplasmic reticulum (ER) stress, and apoptosis in the body. Physical exercise has been a cornerstone in suppressing inflammation and dysmetabolic outcomes caused by TRL4 activation. Thus, the present study aimed to evaluate the effects of a chronic physical exercise protocol on the TLR4 expression and its repercussion in the inflammation, ER stress, and apoptosis pathways in mice hearts. Echocardiogram, RT-qPCR, immunoblotting, and histological techniques were used to evaluate the left ventricle of wild-type (WT) and Tlr4 knockout (TLR4 KO) mice submitted to a 4-week physical exercise protocol. Moreover, we performed a bioinformatics analysis to expand the relationship of Tlr4 mRNA in the heart with inflammation, ER stress, and apoptosis-related genes of several isogenic strains of BXD mice. The TLR4 KO mice had higher energy expenditure and heart rate in the control state but lower activation of apoptosis and ER stress pathways. The bioinformatics analysis reinforced these data. In the exercised state, the WT mice improved performance and cardiac function. However, these responses were blunted in the KO group. In conclusion, TLR4 has an essential role in the inhibition of apoptosis and ER stress pathways, as well as in the training-induced beneficial adaptations. (AU)

FAPESP's process: 20/04269-8 - Role of TLR4 in endoplasmic reticulum stress induced by physical exercise in skeletal muscle
Grantee:Bruno Brieda Marafon
Support Opportunities: Scholarships in Brazil - Master
FAPESP's process: 17/09038-1 - EFFECTS OF REGULAR PHYSICAL EXERCISE AND OVERTRAINING ON THE BEHAVIOR OF THE AUTOPHAGIC PATHWAY IN DIFFERENT TISSUES OF MICE.
Grantee:Adelino Sanchez Ramos da Silva
Support Opportunities: Regular Research Grants