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. Author manuscript; available in PMC: 2015 Mar 28.
Published in final edited form as: J Control Release. 2014 Jan 14;178:8–17. doi: 10.1016/j.jconrel.2014.01.007

Figure 4.

Figure 4

Expression of mature CFTR protein in cells transfected with PEI-MPP carrying CFTR plasmid DNA. (A – C) CFTR protein expression in cells transfected with PEI-MPP carrying pcDNA 3.1 WT-CFTR plasmid DNA (wild-type CFTR). Representative western blots of cultures of (A) primary human airway epithelial cells, (B) CFBE41o- cells stably expressing wild-type CFTR (wtCFTR), and (C) CFBE41o- cells stably expressing ΔF508 CFTR. In each panel, the left lane represents cells treated for 72 h with PEI-MPP carrying pcDNA3.1 WT-CFTR plasmid DNA, whereas the right lane represents untreated controls. Numbers in each panel represent PEI-MPP dose in terms of μg pcDNA3.1 WT-CFTR plasmid DNA. C and B bands exhibit mature, fully glycosylated and immature CFTR protein, respectively. (D – F) Function of expressed CFTR protein in CHO cells treated with PEI-MPP. Representative whole-cell currents from GFP-positive CHO cells transfected with NP carrying pEGFP WT-CFTR plasmid DNA (GFP-wtCFTR) for 72 h (D) before and (E) after bath applications of both 100 μM cAMP and 20 μM forskolin, and (F) after the subsequent addition of 10 μM CFTR inhibitor-172. (G) Current amplitude (I) at 125 mV was significantly increased (*** p < 0.001, n = 5) in PEI-MPP treated cells after the addition of both cAMP and forskolin. The error bars indicate standard error of the mean.