Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery

Mitochondrial biogenesis emerges as a compensatory mechanism involved in the recovery process in endotoxemia and sepsis. The aim of this work was to analyze the time course of the cardiac mitochondrial biogenesis process occurring during endotoxemia, with emphasis on the quantitative analysis of mit...

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Bibliographic Details
Published in:Free radical biology & medicine 2014-12, Vol.77, p.1-9
Main Authors: Vanasco, Virginia, Saez, Trinidad, Magnani, Natalia D., Pereyra, Leonardo, Marchini, Timoteo, Corach, Alejandra, Inés Vaccaro, María, Corach, Daniel, Evelson, Pablo, Alvarez, Silvia
Format: Article
Language:English
Subjects:
Animals
Autophagy
Body Temperature
Endotoxemia
Endotoxemia - immunology
Endotoxemia - metabolism
Female
Lipopolysaccharides - pharmacology
LPS
Microtubule-Associated Proteins - metabolism
Mitochondria, Heart - physiology
Mitochondrial biogenesis
Mitochondrial function
Mitochondrial Turnover
Myocardium - immunology
Myocardium - metabolism
Myocardium - pathology
O2 metabolism
Oxygen Consumption
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Rat heart
Rats, Sprague-Dawley
Transcription Factors - metabolism
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Summary:Mitochondrial biogenesis emerges as a compensatory mechanism involved in the recovery process in endotoxemia and sepsis. The aim of this work was to analyze the time course of the cardiac mitochondrial biogenesis process occurring during endotoxemia, with emphasis on the quantitative analysis of mitochondrial function. Female Sprague-Dawley rats (45 days old) were ip injected with LPS (10mg/kg). Measurements were performed at 0–24h after LPS administration. PGC-1α and mtTFA expression for biogenesis and p62 and LC3 expression for autophagy were analyzed by Western blot; mitochondrial DNA levels by qPCR, and mitochondrial morphology by transmission electron microscopy. Mitochondrial function was evaluated as oxygen consumption and respiratory chain complex activity. PGC-1α and mtTFA expression significantly increased in every time point analyzed, and mitochondrial mass was increased by 20% (P
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2014.08.009