Fig 1: The concentration of PAI-1 in the colonic mucosa. A. Localisation of PAI-1 in the colonic mucosa [blue: nucleus, green: PAI-1, scale bar: 25 µm]. B. Increased ratio of PAI-1 positive cells was detected in the mucosa of inflamed samples [N = 8] compared with non-inflamed tissues [N = 8, p = 0.0126] and controls [N = 8, p = 0.014]. C. The mucosal PAI-1 concentration was significantly higher in the patients with IBD [N = 49] compared with control [N = 19] subjects [p <0.0001]. D. No significant difference was detected between the CD [N = 12] and UC [N = 45] patients [p = 0.7903]. E–F. Significantly increased concentration of PAI-1 was measured in the endoscopically [E] and clinically [F] active [endoscopically active: N = 74, clinically active: N = 62] IBD patients compared with the inactive patients [endoscopically inactive: N = 24, clinically inactive: N = 36] and controls [N = 19] [endoscopically inactive vs active p <0.0001, control vs endoscopically active p <0.0001; clinically inactive vs active p = 0.0015, control vs clinically active p <0.0001]. G. Correlation analysis between the mucosal PAI-1 level and endoscopic disease activity. H–I. ROC analysis of the PAI-1 levels [H] between the inactive [N = 24] and active IBD patients [N = 74] and [I] between the control [N = 19] and active IBD [N = 74] subjects. J–K. After the effective therapy, the mucosal PAI-1 concentration decreased in responders [N = 26]. *p <0.05; **p <0.01; ***p <0.001; ****p <0.0001. IBD-Inflammatory Bowel Disease, CD-Crohn's disease, UC-Ulcerative colitis, PAI-1-Plasminogen activator inhibitor 1
Fig 2: Gene and protein expression of Serpin E1 in human colon organoids. A. Relative gene expression fold change [Fc] of Serpin E1 is not significantly altered in organoid cultures [OCs] generated from active IBD patients [N = 4] and controls [N = 4] [p = 0.3094]. B. Transmission and confocal microscope images of control and IBD OCs. Localisation of the PAI-1 in control and IBD OCs [blue: nucleus, green: PAI-1, scale bar: 25 µm]. C–D. Increased isolated [IBD: N = 4, control: N = 4, p = 0.0286] [C] and secreted [IBD: N = 23, control: N = 14, p = 0.0423]. [D] PAI-1 levels in the IBD OCs compared with the controls. *p <0.05. IBD-Inflammatory Bowel Disease, BACT-Beta-actin.
Fig 3: Stability of the faecal PAI-1 at room temperature and 4°C. RT-Room temperature.
Fig 4: Identification and characterization of protein biomarkers of A-T disease severity. A) Matrixplot of expression of differentially expressed genes across classic A-T and unaffected individuals, restricted to those genes whose protein products are detectable by blood plasma immunoassay or mass-spectrometry according to the Human Protein Atlas. B,D,E) Boxplots of protein concentrations in blood plasma by ELISA for PAI-1 (SERPINE1) (B), VEGFR3 (FLT4) (D), and GP130 (IL6ST) (E), stratified by condition. C) Linear regression of PAI-1 plasma concentration versus age in individuals with classic A-T
Fig 5: Faecal PAI-1 concentration in organic gastrointestinal diseases. Increased PAI-1 levels were detected in faecal samples of active IBD patients [N = 86] compared with patients with organic gastrointestinal diseases [control: N = 29, p <0.0001; inactive IBD: N = 60, p <0.0001; adenoma: N = 15, p = 0.0346; colorectal cancer: N = 8, p <0.0001; diverticulosis: N = 9, p = 0.0005]. IBD-Inflammatory Bowel Disease, CRC-Colorectal cancer.
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