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. 2013 Oct;49(4):672–679. doi: 10.1165/rcmb.2013-0156OC

Figure 3.

Figure 3.

Functional cystic fibrosis transmembrane conductance regulator (CFTR) is needed for H2O2-induced ∆ISC. NHBE cells, fully differentiated at the ALI, were mounted in Ussing chambers, and treated apically with amiloride, followed by either apical 4,4′-dinitrostilbene-2,2′-disulfonic acid (100 μM, n = 4 cultures from three lung donors), apical CFTRinh-172 (5 μM, n = 5 cultures from four lung donors), or apical GlyH-101 (10 μM, n = 8 cultures from seven lung donors), and then stimulation with either 1 mM or 50 μM H2O2 in the apical compartment. (a) CFTRinh-172 and GlyH-101 significantly blocked the H2O2-induced ∆ISC at 1 mM. CFTRinh-172 (5 μM, n = 8 cultures from five lung donors) and GlyH-101 (10 μM, n = 3 lung donors) also blocked responses at 50 μM (a). (b) A representative trace with CFTRinh-172 (5 μM, solid line) and control trace (dotted line) at 1 mM H2O2. Fully differentiated cystic fibrosis bronchial epithelial (CFBE) culture did not increase ISC after apical 1 mM H2O2 treatment (c, bottom trace in gray). (c) CFBE not treated with H2O2 (top trace). (d) A representative trace with GlyH-101 (10 μM, solid line) and a control trace (dotted line) at 1 mM H2O2. Values represent means ± SEMs. *P < 0.05.