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FEBS Lett. 2011 Oct 3;585(19):3065-72. doi: 10.1016/j.febslet.2011.08.029. Epub 2011 Aug 26.

Differential requirement for nitric oxide in IGF-1-induced anti-apoptotic, anti-oxidant and anti-atherosclerotic effects.

Author information

1
Tulane University Heart & Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, USA. ssukhano@tulane.edu

Abstract

We have shown previously that insulin like-growth factor I (IGF-1) suppressed atherosclerosis in Apoe(-/-) mice and activated endothelial nitric oxide (NO) synthase. To determine whether IGF-1-induced atheroprotection depends on NO, IGF-1- or saline-infused mice were treated with l-NAME, the pan-NO synthase inhibitor or with d-NAME (control). IGF-1 reduced atherosclerosis in both the d-NAME and l-NAME groups suggesting that IGF-1's anti-atherogenic effect was NO-independent. IGF-1 increased plaque smooth muscle cells, suppressed cell apoptosis and downregulated lipoprotein lipase and these effects were also NO-independent. On the contrary, IGF-1 decreased oxidative stress and suppressed TNF-α levels and these effects were blocked by l-NAME. Thus IGF-1's anti-oxidant effect is dependent on its ability to increase NO but is distinct from its anti-atherosclerotic effect which is NO-independent.

PMID:
21872589
PMCID:
PMC3183325
DOI:
10.1016/j.febslet.2011.08.029
[Indexed for MEDLINE]
Free PMC Article

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