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Hepatology. 2010 Dec;52(6):2137-47. doi: 10.1002/hep.23909. Epub 2010 Oct 7.

Interleukin-6 is an important mediator for mitochondrial DNA repair after alcoholic liver injury in mice.

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  • 1Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Abstract

We investigated the hypothesis that a prominent effect of chronic ethanol consumption is mitochondrial DNA (mtDNA) injury and compared this injury in IL-6 knockout (KO) and wild-type (WT) mice. Ethanol feeding for 4 weeks resulted in steatosis and oxidative mtDNA damage (8-OHdG) in both IL-6KO and WT mice. However, the WT mice were able to repair the injury by increased production of mtDNA repair enzymes (OGG-1, Neil 1) and check point (p21, p53) proteins and avoid the mtDNA mutations. By contrast the IL-6 KO mice were unable to repair mtDNA resulting in deletions and diminished transcription of the mtDNA encoded protein cytochrome c oxidase subunit-I (COI). The mitochondrial injury was reflected by decreased membrane potential, reduced levels of ATP, and apoptosis-inducing factor (AIF)-induced apoptosis.

CONCLUSION:

IL-6 plays a critical role in allowing the liver to recover from significant mtDNA oxidation caused by alcohol. The data suggests that IL-6 activates mtDNA repair enzymes and induces cell cycle arrest allowing time for mtDNA repair.

Copyright © 2010 American Association for the Study of Liver Diseases.

PMID:
20931558
[PubMed - indexed for MEDLINE]
PMCID:
PMC2991528
Free PMC Article

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