Research Paper Advance Articles pp 24301—24317

Cigarette smoke extract induces airway epithelial cell death via repressing PRMT6/AKT signaling

Figure 4. CSE downregulates PI3K/AKT signal transduction in lung epithelial cells. (A) BEAS-2B cells were treated with 6% CSE for 0, 2, 4, 6h. Cell lysates were immunoblotted with phosphorylated AKT and total AKT. The densitometry results of the blots were presented in the lower panel. (B) HSAECs cells were treated with 8% CSE in a range of concentrations as indicated for 0, 2, 4, 8h. Phosphorylated AKT and AKT3 were immunoblotted. The densitometry of the blots was presented in its lower panel. (C) HSAECs were applied to room air or cigarette smoke exposure. RA: room air; CS: cigarette smoke. Cell lysates were immunoblotted with pAKTThr305, pAKTSer472, AKT3 and GAPDH antibodies. The densitometry results of the blots were presented in the lower panel. (D) Both WT and PRMT6-/- BEAS-2B cells were treated with CSE at different time courses. Cell lysates were subjected to immunoblotting with pAKTThr305, pAKTSer472, AKT3, PRMT6, and GAPDH. Results were shown as mean ± SD and representative of n=3 experiments. Statistical significance was indicated as *: p < .05.