Fig 1: Plasma claudin-5 (CLDN5) is elevated in thoracic aortic aneurysm and dissection (TAAD) patients. (a) Plasma CLDN5 concentrations in TAAD patients (N = 44, red) and healthy controls (CTL, N = 41, green). * p < 0.05 using Welch’s t test; (b) Correlation between plasma CLDN5 levels and systolic blood pressure (SBP) in TAAD patients (N = 44); (c) CLDN5 levels relative to time before symptom onsets (CTL, N = 41; time ≤ 1-day, N = 22; time > 1-day and ≤7-day, N = 15; time > 7-day, N = 7). * p < 0.05 using the Kruskal–Wallis test with Dunn’s multiple comparisons test; (d) ROC curve analysis evaluating the diagnostic performance of CLDN5 for TAAD.
Fig 2: Schematic summarizing the role of CLDN5 in thoracic aortic aneurysm and dissection (TAAD). Under physiological conditions, endothelial cells (ECs) form intact tight junctions (TJs), with CLDN5 maintaining endothelial barrier integrity. In TAAD, inflammatory stimuli (e.g., TNF-α) induce the proteolytic cleavage of CLDN5 by proteases, disrupting TJs and releasing CLDN5 fragments into circulation as potential biomarkers.
Fig 3: Structural profiling of claudin-5 (CLDN5) reveals a four-pass transmembrane protein with defined regulatory features: (a) CpG island analysis of the CLDN5 gene identifying two islands (positions 560–1109, length 550 bp; and 118–2028, length 848 bp) across the analyzed sequence (1–2332 bp); (b) Predicted membrane topology of CLDN5 generated using the Phobius database. Transmembrane domains are shown in purple, intracellular regions in green, and extracellular regions in blue; (c) Secondary structure and disorder propensity predictions; (d) Schematic illustrating the predicted domain architecture of CLDN5 protein.
Fig 4: Tumor necrosis factor-α (TNF-α) disrupts endothelial barrier integrity through claudin-5 (CLDN5) release and functional impairment: (a) Immunofluorescence images showing CLDN5 expression (red) in human umbilical vein endothelial cells (HUVECs) with or without TNF-α stimulation. Nuclei were counterstained with DAPI (blue). Data are presented as the mean ± SEM and analyzed by using an unpaired two-tailed Student’s t test. N = 4 per group. Scale bar = 20 μm. * p < 0.05; (b) CLDN5 concentrations in HUVECs culture supernatants with or without TNF-α stimulation quantified via ELISA. Data are presented as the mean ± SEM and analyzed by using an unpaired two-tailed Student’s t test. N = 4 per group. * p < 0.05; (c) Transendothelial electrical resistance (TER) of HUVECs under control conditions and after CDLN5 knockdown. Data are presented as the mean ± SEM and analyzed by using an unpaired two-tailed Student’s t test. N = 7 per group. * p < 0.05. (d) Paracellular permeability assay assessed using 4 kDa FITC-dextran in HUVECs under control conditions and after CDLN5 knockdown. Data are presented as the mean ± SEM and analyzed by using an unpaired two-tailed Student’s t test. N = 5 per group. * p < 0.05.
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