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IGF1 — NOS3

Text-mined interactions from Literome

Michell et al., Curr Biol 1999 : Preincubation with wortmannin, an inhibitor of Akt signalling, reduced VEGF- or IGF-1 induced Akt activity and eNOS phosphorylation
Guan et al., Neuroscience 2000 (Brain Ischemia) : Insulin-like growth factor-1 markedly prevented the loss of calbindin-28kd ( n = 7, P < 0.05 ), choline acetyltransferase ( n = 7, P < 0.05 ), neuropeptide Y ( n = 7, P < 0.05 ), neuronal nitric oxide synthase ( n = 8, P < 0.05 ) and glutamate acid decarboxylase ( n = 9, P < 0.05 ) immunopositive neurons, but failed to protect parvalbumin ( n = 6 ) immunopositive neurons
Castrillo et al., Diabetes 2000 : Inhibitory effect of IGF-I on type 2 nitric oxide synthase expression in Ins-1 cells and protection against activation dependent apoptosis : involvement of phosphatidylinositol 3-kinase
Isenović et al., Biochem Biophys Res Commun 2001 : Role of PI3-kinase in isoproterenol and IGF-1 induced ecNOS activity
Isenović et al., Metabolism 2002 : In addition, Iso as well as IGF-1 significantly increased eNOS activity measured by nitrite production
Isenovic et al., Metabolism 2003 : Interactive effects of insulin-like growth factor-1 and beta-estradiol on endothelial nitric oxide synthase activity in rat aortic endothelial cells
Wang et al., Nitric Oxide 2004 (Diabetic Nephropathies) : Stimulatory effect of IGF-I and VEGF on eNOS message, protein expression, eNOS phosphorylation and nitric oxide production in rat glomeruli, and the involvement of PI3-K signaling pathway ... Our data suggest the great possibility that increased endogenous IGF-I and VEGF may be responsible for the up-regulation of eNOS expression and NO production which contributes to glomerular hyperfiltration in early diabetic kidneys
Repetto et al., Biochem Biophys Res Commun 2005 : Since Insulin and IGF-I phosphorylate and activate eNOS , we investigated the role of caveolin-1 in Insulin and IGF-I stimulated eNOS activity ... Here we show that : ( 1 ) in human endothelial cells, Insulin and IGF-I stimulate eNOS phosphorylation in a different manner both qualitatively and quantitatively ; ( 2 ) caveolin-1 down regulation abolishes Insulin and IGF-I stimulated eNOS phosphorylation ... These results suggest that caveolae could represent an intracellular site that contributes to differentiate IR and IGF-IR activity, and demonstrate the role of caveolin-1 in the eNOS activation by Insulin and IGF-I
Thum et al., Circ Res 2007 : IGF-1 increased telomerase activity, endothelial nitric oxide synthase expression, phosphorylation and activity in EPC in a phosphoinositide-3-kinase/Akt dependent manner
Sukhanov et al., Arterioscler Thromb Vasc Biol 2007 (Atherosclerosis...) : Furthermore, IGF-1 decreased vascular expression of the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, reduced aortic superoxide formation and urinary 8-isoprostane levels, and increased aortic pAkt and eNOS expression and circulating endothelial progenitor cells, consistent with an antiinflammatory, antioxidant, and prorepair effect on the vasculature
Imrie et al., Endocrinology 2009 (Insulin Resistance...) : IGF-I increased NO synthase activity to an extent similar to that seen with insulin and in-vivo IGF-I led to serine phosphorylation of endothelial NO synthase (eNOS) ... IGF-I increased aortic phospho-eNOS levels in lean mice, an effect that was blunted in obese mice ... eNOS activity in aortae of lean mice increased 1.6-fold in response to IGF-I compared with obese mice
Stone et al., J Gerontol A Biol Sci Med Sci 2012 : Moreover, IGF-1 also activated endothelial nitric oxide synthase in human umbilical vein endothelial cells