Figure 5. Functional impact of 11βPGF₂α on IEB healing.

IEC properties were evaluated in Caco-2 monolayers after three days of culture in presence of lipid mediator 11βPGF₂α or not (CT).(a) Representative pictures of epithelial healing of IEC monolayers cultured without treatment (CT) or with 11βPGF₂α for two days. (b) Quantification of epithelial healing was calculated as a percentage of healing between t0 and 48 h. n = 5–12; Kruskal-Wallis test; *p < 0.05 as compared to IEC without treatment. (c) Epithelial spreading was expressed as percentage of CT IEC surface. n = 5–8 independent experiments performed in duplicates; Kruskal-Wallis test; ***p < 0.005 as compared to CT. (d) IEC properties were also evaluated in Caco-2 monolayers after two days of co-culture with Control EGC or CD EGC in presence of the lipid mediator 11βPGF₂α or not (−). Quantification of epithelial healing was calculated as a percentage of healing between t0 and 48 h. n = 3; Kruskal-Wallis test; *p < 0.05 as compared to CD EGC-Caco2 co-cultures without treatment. ^§p < 0.05 as compared to Control EGC-Caco2 co-cultures without treatment. (e) PPARγ immunostaining on Caco-2 treated 5min with 11βPGF₂α compared to ZO-1 staining. n = 3 independent experiments, scale 20 μM. (f) Western blotting analyzes of PPARγ expression in Caco-2 treated 24 hours with 11βPGF₂α. (g) Quantification of PPARγ/β-actin related to the average control ratio taken as 1. Data represent mean ± SEM, n = 4 independent experiments; Kruskal-Wallis test; *p < 0.05 as compared to cont.