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J Biol Chem. 2013 Jan 25;288(4):2246-60. doi: 10.1074/jbc.M112.375253. Epub 2012 Dec 8.

The peroxisome proliferator-activated receptor γ coactivator 1α/β (PGC-1) coactivators repress the transcriptional activity of NF-κB in skeletal muscle cells.

Author information

1
Biozentrum, Division of Pharmacology/Neurobiology, University of Basel, CH-4056 Basel, Switzerland.

Erratum in

  • J Biol Chem. 2013 Mar 1;288(9):6589.

Abstract

A persistent, low-grade inflammation accompanies many chronic diseases that are promoted by physical inactivity and improved by exercise. The beneficial effects of exercise are mediated in large part by peroxisome proliferator-activated receptor γ coactivator (PGC) 1α, whereas its loss correlates with propagation of local and systemic inflammatory markers. We examined the influence of PGC-1α and the related PGC-1β on inflammatory cytokines upon stimulation of muscle cells with TNFα, Toll-like receptor agonists, and free fatty acids. PGC-1s differentially repressed expression of proinflammatory cytokines by targeting NF-κB signaling. Interestingly, PGC-1α and PGC-1β both reduced phoshorylation of the NF-κB family member p65 and thereby its transcriptional activation potential. Taken together, the data presented here show that the PGC-1 coactivators are able to constrain inflammatory events in muscle cells and provide a molecular link between metabolic and immune pathways. The PGC-1s therefore represent attractive targets to not only improve metabolic health in diseases like type 2 diabetes but also to limit the detrimental, low-grade inflammation in these patients.

PMID:
23223635
PMCID:
PMC3554897
DOI:
10.1074/jbc.M112.375253
[Indexed for MEDLINE]
Free PMC Article

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