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Cardiovascular Research 2004 64(2):279-288; doi:10.1016/j.cardiores.2004.07.005
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Lipopolysaccharide induces oxidative cardiac mitochondrial damage and biogenesis

Hagir B. Sulimana,b, Karen E. Welty-Wolfa, MarthaSue Carrawaya, Lynn Tatroa and Claude A. Piantadosia,b,*

aDepartment of Medicine, Duke University Medical Center, 0590 CR II Building, Duke South Hospital Trent Drive, Durham, NC 27710, United States
bDepartment of Anesthesiology, Duke University Medical Center, Durham, NC 27710, United States

* Corresponding author. Tel.: +1 919 684 8908; fax: +1 919 684 6002. Email address: piant001{at}mc.duke.edu

Objective: The responses to bacterial lipopolysaccharide (LPS) damage mitochondria by generating oxidative stress within the organelles. We postulated that LPS damages heart mitochondrial DNA and protein by oxidation, and that this is recovered by oxidative mechanisms of mitochondrial biogenesis.

Methods and results: Systemic crude E. coli LPS administration decreased mtDNA copy number and mtDNA gene transcription in rat heart caused by oxidant deletion of mtDNA. The fall in copy number was reflected in proteomic expression of several mitochondria-encoded subunits of Complexes I, IV, and V. Recovery of mtDNA copy number involved biogenesis as indicated by mitochondrial transcription factor A (Tfam) and DNA polymerase-{gamma} expression. The transcriptional response also included nuclear accumulation of peroxisome proliferator-activated receptor-{gamma} co-activator 1 (PGC-1) and mRNA expression for redox-regulated nuclear respiratory factors (NRF-1 and -2).

Conclusions: These novel findings disclose a duality of reactive oxygen species (ROS) effect in the heart’s response to LPS in which oxidative mitochondrial damage is opposed by oxidant stimulation of biogenesis.

KEYWORDS Infection/inflammation; Sepsis; Mitochondria; Oxygen radicals; Redox signaling

Time for primary review 16 days


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