Fig. 4
TMIGD1 downregulation aggravates inflammation and weakens intestinal epithelial barrier function in the inflammatory environment. A Transcriptomic analysis of genes related to epithelial barrier function and inflammatory cytokines in the colonic tissues of WT+DSS and Tmigd1INT-KO+DSS mice. B The differentiated genes were enriched in barrier function and inflammation-relevant cytokines according to gene ontology (GO) analysis. C Myeloperoxidase (MPO) activity in colon tissues; WT+water (n=8), Tmigd1INT-KO+water (n=8), WT+DSS (n=10), Tmigd1INT-KO+DSS (n=12); WT+Alcohol (n=10), Tmigd1INT-KO+Alcohol (n=10), WT+TNBS (n=10), Tmigd1INT-KO+TNBS (n=15). D Serum TNF-α and IL-6 concentrations were tested using multiELISA; Every group, n=5. E The concentration of serum FD4; WT+water (n=5), Tmigd1INT-KO+water (n=5), WT+DSS (n=6), Tmigd1INT-KO+DSS (n=8). F Measurement of microvilli length and AJC gaps in colonic epithelial cells using TEM. Every group, n=3. G Representative TEM images of the colonic mucosa. The arrowheads indicate AJC. Scale bars, 500 nm. H, I TEER and FD4 permeability of Caco2 monolayer cell model after TNF-α stimulation. J, K The expression of AJC proteins (J) and inflammation-relevant cytokine mRNA and AJC mRNA (K) in NCM460 cells after TNF-α stimulation. L After TNF-α treatment, FD4 permeability of human colonic organoids was detected using confocal microscopy. Scale bars, 100 μm. M The FD4 permeability of colonic organoids from Tmigd1INT-KO and WT mice was detected using confocal microscopy before and after TNF-α treatment. Scale bars, 100 μm. Data are expressed as mean ± SEM. ns, no significance, * p<0.05, ** p<0.01, *** p<0.001