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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Vascul Pharmacol. 2015 Apr 25;73:20–31. doi: 10.1016/j.vph.2015.04.005

Figure 2. IGF-1 activates pAKT in PASMC.

Figure 2

(A) IGF-1 increases pAKTS473 in mouse PASMC. PASMC were serum-starved overnight and then incubated with IGF-1 (100 ng/ml) for 24 h. Cell lysates were prepared and subjected to Western blot analysis using an antibody against pAKTS473. Pan AKT and β-actin were used as loading controls. (B) Densitometry quantification of pAKTS473 levels in the mPASMC in the presence or absence of IGF-1 for Figure 1A. * p<0.05 compared with the untreated control. (C) Inhibitors of IGF-1R (OSI-906), AKT (MK-2206), and PI3K (PF-04691502) decrease IGF-1-induced pAKT473 in HPASMC. However, inhibitors of AKT (MK-2206) and PI3K (PF-04691502) are capable of decreasing the levels of pAKTT308, while the IGF-1R inhibitor (OSI-906) is not. (D) Densitometry quantification of pAKTS473 levels for Figure 2C. * p<0.05 compared with the untreated control. # p<0.05 compared to IGF-1-treated control (IGF-1 +, no inhibitor).