Dysregulated signal transducer and activator of transcription 3 drives intestinal permeability and may contribute to acute-on-chronic liver failure

Figure 6 Identification of signal transducer and activator of transcription 3-dependent differences of lipid species by liquid chromatography high-resolution mass spectrometry analysis. Caco-2 and T84 cell monolayers were generated over a period of 28 days. Thereafter, cells were harvested and lipidomic analysis was performed. A and B: Venn diagrams illustrate the number of significantly altered lipid species in decreased signal transducer and activator of transcription 3 (STAT3) (STAT3 -) and enhanced STAT3 (STAT3 +) expressing Caco-2 and T84 cell monolayers compared to the controls. The overlapping area represents lipids significantly regulated in both epithelial models, indicating STAT3-dependent lipid remodeling; C and D: Bars show all lipid species that were significantly changed in Caco-2 as well as T84 monolayers (see also A and B), respectively. Bars represent mean log₂ fold change ± SEM. Cross-validation across two independent intestinal epithelial models ensures robustness and minimizes false-positive discovery. P < 0.05, two-sided Welch’s t-test (n = 5). STAT3: Signal transducer and activator of transcription 3; PG: Phosphatidylglycerol; LPC: Lysophosphatidylcholines; PC: Phosphatidylcholine; TG: Triacylglycerol; SM: Sphingomyelin; PC O: Ether-linked phosphatidylcholine; TG O: Ether-linked triacylglycerol.