Akt1/protein kinase Bα is critical for ischemic and VEGF-mediated angiogenesis
J. Clin. Invest. Eric Ackah, et al. 115:2119 doi:10.1172/JCI24726 [Go to this article.]

Figure 6
Impaired cell migration and NO release in Akt1^–/– cells. (A) Migration of MLECs was examined in modified Boyden chambers using sphingosine-1-phosphate (S-1-P) as a chemoattractant. Migration of Akt1^–/– cells was reduced at all doses examined. Data are mean ± SEM; n = 4 from 3 independent experiments. (B) Migration of lung fibroblasts was examined in the modified Boyden chamber using serum-free DMEM (Basal) or 10% FBS as agonist. (C) Basal production of NO in MLECs (assayed as NO₂^– in the media) over a 24-hour period was determined by chemiluminescence. Levels of NO₂^– in media alone were subtracted out. (D) Cells were stimulated with VEGF (50 ng/ml) for 30 minutes, and NO release was quantified by chemiluminescence. For stimulated NO₂^– release, values were calculated by subtracting out levels obtained with nonstimulated cells. Data are mean ± SEM; n = 9–12 from 3 independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.