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. 2019 May 2;151(6):834–849. doi: 10.1085/jgp.201812143

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© 2019 Abu-Arish et al.

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Figure 7. — VIP increases CFTR retention at the plasma membrane through a lipid-dependent mechanism. (A) EGFP-CFTR fluorescence ratio at the surface of subconfluent pHBE cells normalized to the control fluorescence before VIP stimulation. Fluorescence was increased ∼60% by VIP (P < 0.001), and this response was prevented by pretreating cells with COase to disrupt lipid rafts, or with Ami to inhibit ceramide synthesis. (B–D) CSB of CFTR in CFBE41o⁻ cells. (B) Shows no effect of VIP stimulation on total CFTR expression or Na⁺/K⁺ ATPase α subunit (loading control) in whole cell lysates but reveals an 80% increase in CFTR that is CSB after VIP stimulation. (C) Pretreatment with COase or Ami individually prevents the VIP-induced increase in cell surface CFTR. (D) Summary of surface biotinylation results under Ctr conditions and with VIP. Inset: Exposure to VIP alone induces small EGFP-CFTR platforms in CFBE41o⁻ cells. (E) Inhibiting ceramide synthesis blunts VIP-stimulated and also FSK-stimulated short-circuit current responses (ΔI_sc). (F) I_sc traces recorded using basolaterally permeabilized CFBE41o⁻ cells and an apical-to-basolateral Cl⁻ gradient to functionally remove the basolateral membrane. (G) Summary of I_sc responses to VIP in basolaterally permeabilized CFBE41o⁻ cells showing that VIP stimulation under these conditions was also inhibited 40–45% by Ami pretreatment. (H) VIP- and FSK- stimulated I_sc across pHBE cells was reduced 43% and 38% by pretreatment with Ami, respectively. n = 8–12 filters/condition. Mean ± SEM, *, P < 0.025; **, P < 0.01; ***, P < 0.001. Nys, nystatin; Inh, inhibitor.