Figure 4.
Effects of protease inhibitors on ER stress-induced epithelial dysfunction in enterocytes. [A–C] Monolayers of differentiated Caco-2 cells were cultivated in a transwell system, and were stimulated with Thapsigargin [Tg; 10 µg/mL] for 6 h in the presence or not of trypsin inhibitors (AEBSF [200 µM] or Leupeptin [50 µM]). [A] Paracellular permeability was monitored by measuring the apical-to-basolateral flux of dextran 4kDa–FITC. [B] Relative mRNA expressions of β-Defensin-1, β-Defensin-2, Trefoiled factor-3, mucin-2, CXCL8 and TNFα after 6 h of ER stress stimulation. [C] Levels of CXCL8, β-Defensin-2, Trefoiled factor-3 and mucin-2 monitored by ELISA, and released by Caco-2 cells in the apical and basolateral compartments of the transwell system. Data expressed as mean ± SEM were compared using one-way non-parametric ANOVA [Bonferroni test]. **p < 0.01, ***p < 0.001, ****p < 0.0001 vs Control group; ϕp < 0.05, ϕϕp < 0.01, ϕϕϕp < 0.001, ϕϕϕϕp < 0.0001 vs Thapsigargin group.

Effects of protease inhibitors on ER stress-induced epithelial dysfunction in enterocytes. [A–C] Monolayers of differentiated Caco-2 cells were cultivated in a transwell system, and were stimulated with Thapsigargin [Tg; 10 µg/mL] for 6 h in the presence or not of trypsin inhibitors (AEBSF [200 µM] or Leupeptin [50 µM]). [A] Paracellular permeability was monitored by measuring the apical-to-basolateral flux of dextran 4kDa–FITC. [B] Relative mRNA expressions of β-Defensin-1, β-Defensin-2, Trefoiled factor-3, mucin-2, CXCL8 and TNFα after 6 h of ER stress stimulation. [C] Levels of CXCL8, β-Defensin-2, Trefoiled factor-3 and mucin-2 monitored by ELISA, and released by Caco-2 cells in the apical and basolateral compartments of the transwell system. Data expressed as mean ± SEM were compared using one-way non-parametric ANOVA [Bonferroni test]. **p < 0.01, ***p < 0.001, ****p < 0.0001 vs Control group; ϕp < 0.05, ϕϕp < 0.01, ϕϕϕp < 0.001, ϕϕϕϕp < 0.0001 vs Thapsigargin group.

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