Differential requirement for nitric oxide in IGF-1-induced anti-apoptotic, anti-oxidant and anti-atherosclerotic effects |
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Authors: | Sukhanov Sergiy Higashi Yusuke Shai Shaw-Yung Blackstock Christopher Galvez Sarah Vaughn Charlotte Titterington Jane Delafontaine Patrick |
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Affiliation: | Tulane University Heart & Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, USA. ssukhano@tulane.edu |
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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. |
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