Skip to main content
Fig. 4 | Biology Direct

Fig. 4

From: The CXCR3/PLC/IP3-IP3R axis is responsible for the ignition of UPR in intestinal epithelial cells exposed to gliadin peptide, during the onset of celiac disease

Fig. 4

CXCR3 is required to deregulate TJ proteins expression. Gadd153 enhances the expression of CXCR3, under PT stimulation. The expression of CXCR3 was evaluated in both CaCo-2 cells (A) or s.i. (B) unexposed (CTRL) or exposed to PT (1 mg/mL, 9 h, in CaCo-2; 5 mg/mL, 16 h, in GEVS) alone or in combination with 4PBA (3 M and 5 M, respectively) by qPCR. The expression of Gadd153 was evaluated in both CaCo-2 cells (C) or s.i. (D) unexposed (CTRL) or exposed to PT (1 mg/mL, 9 h, in CaCo-2; 5 mg/mL, 16 h, in GEVS) by qPCR. CaCo-2 cells were unexposed (CTRL) or exposed 9 h to PT (1 mg/mL), AEBSF (500 M), GSK2606414 (GSK, 5 M), or STF-083010 (STF, 60 M) alone or in combination, and the expression of Gadd153 (E), and CXCR3 (F) was evaluated by qPCR. CaCo-2 cells were transfected with vectors carrying two shRNA specific sequences (shGadd153#29; shGadd153#93; using a scrambled sequence as a control, shCR), and the expression of both Gadd153 (G) and CXCR3 (H) was evaluated by qPCR, in cells unexposed (CTRL) or exposed to PT (1 mg/mL, 9 h). A schematic representation of the mechanism by which gliadin peptides regulate the expression of CXCR3 is shown (I). Data are representative of three independent experiments performed in triplicate. Histograms represent mean ± s.d.; ****p < 0.0001 (vs. control); •••• p < 0.0001

Back to article page