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. 2016 Feb 10;11(2):e0149131. doi: 10.1371/journal.pone.0149131

Fig 5. CP7q potentiates G551D-CFTR in FRT cells and WT-CFTR in primary cultured human nasal epithelial cells.

Fig 5

(A) Apical membrane currents were measured in FRT cells expressing human G551D-CFTR. CFTR was stimulated by application of 20 μM forskolin and then 50 μM genistein (left panel), 10 μM VX-770 (middle panel) or indicated concentrations of CP7q (right panel) were applied to bath solution. CFTR-dependent current was inhibited by 10 μM CFTRinh-172. (B) Summary of CP7q-induced fold increase in G551D-CFTR current stimulated by 20 μM forskolin (mean ± S.E., n = 3). (C) Summary of 50 μM genistein, 10 μM VX-770 and 30 μM CP7q induced peak current (mean ± S.E., n = 3). (D) Short-circuit currents were measured in normal human nasal epithelial cells (left panel). CFTR was activated by 0.5 μM forskolin. CFTR was potentiated by indicated concentrations of CP7q and inhibited by 10 μM CFTRinh-172. ENaC was inhibited by 100 μM amiloride. Bar graph showing the summarized data of peak current (mean ± S.E., n = 3, right panel). **P < 0.01.