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Title 

Mitochondrial dysfunction induces formation of lipid droplets as a generalized response to stress

Authors 

Seon-Jin LeeJ ZhangA M K ChoiH P Kim

Publisher 

Landes Bioscience

Issue Date 

2013

Citation 

Oxidative Medicine and Cellular Longevity, vol. 2013, no. 0, pp. 327167-327167

Abstract 

Lipid droplet (LD) formation is a hallmark of cellular stress. Cells attempt to combat noxious stimuli by switching their metabolism from oxidative phosphorylation to glycolysis, sparing resources in LDs for generating cellular reducing power and for anabolic biosynthesis. Membrane phospholipids are also a source of LDs. To elucidate the formation of LDs, we exposed mice to hyperoxia, hypoxia, myocardial ischemia, and sepsis induced by cecal ligation and puncture (CLP). All the above-mentioned stressors enhanced the formation of LDs, as assessed by transmission electron microscopy, with severe mitochondrial swelling. Disruption of mitochondria by depleting mitochondrial DNA (ρ0 cells) significantly augmented the formation of LDs, causing transcriptional activation of fatty acid biosynthesis and metabolic reprogramming to glycolysis. Heme oxygenase (HO)-1 counteracts CLP-mediated septic shock in mouse models. In HO-1-deficient mice, LD formation was not observed upon CLP, but a concomitant decrease in "LD-decorating proteins" was observed, implying a link between LDs and cytoprotective activity. Collectively, LD biogenesis during stress can trigger adaptive LD formation, which is dependent on mitochondrial integrity and HO-1 activity; this may be a cellular survival strategy, apportioning energy-generating substrates to cellular defense.

ISSN 

1942-0900

Link 

http://dx.doi.org/10.1155/2013/327167

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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