Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells
J. Clin. Invest. Kip A. West, et al. 111:81 doi:10.1172/JCI16147 [Go to this article.]

Figure 4
Nicotine-mediated Akt activation and survival of NHBEs. (a) Topoisomerase II inhibition. Nicotine (10 μM) protected against etoposide-induced apoptosis, as assessed by flow cytometry. Pretreatment with LY294002 decreased nicotine-mediated survival. Parallel samples were harvested for immunoblotting (inset; C, control; N, nicotine; LY, LY294002; LY/N, LY294002 + nicotine). (b) UV irradiation. Nicotine (10 μM) protected against UV irradiation–induced apoptosis, as measured using CellDeath ELISA kits. Pretreatment with LY294002 or DHβE attenuated nicotine-mediated survival. (c and d) H₂O₂ treatment. NHBEs were pretreated with nicotine (10 μM) (c) or NNK (d) as above, with or without H₂O₂ (200 μM). After 4 hours, cells were harvested, dead cells that exhibited cytoplasmic inclusion of 0.4% trypan blue were counted, and this number was compared with the total number of cells. At least 300 cells per sample were counted by a blinded observer.