Fig. 3: Effects of EoE-associated DSP and PPL variants.

a Representative hematoxylin and eosin (H&E)–stained sections of EPC2 cells stably transduced with constructs encoding non-variant and mutated DSP or PPL after air–liquid interface (ALI) differentiation (day 14). Arrows point to the non-cellular areas that were formed. Scale bar: 50 μM. Data are representative of three experiments performed in duplicate. b The transepithelial electrical resistance (TEER) and c FITC-dextran flux measurements are shown for EPC2 cells grown at the ALI. d Wound healing assays performed in EPC2 cells transduced with constructs encoding non-variant and mutated DSP or PPL. Quantification of the wound closure after 8 h was shown. For panels b–d data are representative of three experiments performed in duplicate and are presented as mean ± SEM. Statistics (versus non-variants): b (p.G46D, P = 0.0324; p.R808C, P = 0.0059; p.Y895C, P = 0.0042; p.1067_1068del, P = 0.0006; p.N1215S, P = 0.0005; p.R1340C, P = 0.0003; p.E1723Q, P = 0.0012; p.R108C, P = 0.0041; p.E632K, P = 0.0131; p.K1051V, P = 0.0189; p.L1154V, P = 0.0004; p.E1163K, P = 0.0024; p.V1377E, P = 0.0291), c (p.G46D, P = 0.1542; p.R808C, P = 0.0274; p.Y895C, P = 0.0151; p.1067_1068del, P = 0.0062; p.N1215S, P = 0.1189; p.R1340C, P = 0.0244; p.E1723Q, P = 0.0385; p.R108C, P = 0.0187; p.E632K, P = 0.066; p.K1051V, P = 0.0536; p.L1154V, P = 0.0022; p.E1163K, P = 0.0304; p.V1377E, P = 0.1601) and d (p.G46D, P = 0.9917; p.R808C, P = 0.0103; p.Y895C, P = 0.005; p.1067_1068del, P = 0.0031; p.N1215S, P = 0.0944; p.R1340C, P = 0.0187; p.E1723Q, P = 0.4656; p.R108C, P = 0.0249; p.E632K, P = 0.0748; p.K1051V, P = 0.9471; p.L1154V, P = 0.0016; p.E1163K, P = 0.0194; p.V1377E, P = 0.9261). For panels b–d, two-tailed P-values were determined by the one-way ANOVA test followed by a Dunnett’s multiple-comparison test. *P < 0.05, **P < 0.01, and ***P < 0.001. EoE eosinophilic esophagitis, DSP desmoplakin, PPL periplakin, FITC fluorescein isothiocyanate, SEM standard error of the mean.