Fig 1: Endothelial pro-inflammatory protein secretion in EA.hy926 cells and HUVECs incubated for 24 h with macrophage-conditioned media. THP-1–derived unpolarized, M1-like, and M2-like macrophages were exposed to normoxia (N), chronic hypoxia (chH), or cycling hypoxia (cyH) for 6 h and were then left for 16 h in normoxic air to produce macrophage-conditioned media. Thereafter, EA.hy926 cells (A) and HUVECs (B) were incubated for 24 h with macrophage-conditioned media and the secretion of IL-6, IL-8, and ESM1 in the endothelial cells was assessed by ELISA (n = 3, mean ± 1 SEM). Ctrl corresponds to endothelial cells incubated with CO2-independent medium. Statistical analysis was performed using Student’s t test. *p < 0.05.
Fig 2: Endothelial pro-inflammatory mRNA expression in EA.hy926 cells and HUVECs incubated for 24 h with macrophage-conditioned media. THP-1–derived unpolarized, M1-like, and M2-like macrophages were exposed to normoxia (N), chronic hypoxia (chH), or cycling hypoxia (cyH) for 6 h and were then left for 16 h in normoxic air to produce macrophage-conditioned media. Thereafter, EA.hy926 cells (A) and HUVECs (B) were incubated for 24 h with macrophage-conditioned media and their mRNA expression for IL-6, IL-8, and ESM1 was assessed by RT-qPCR (n = 4, mean ± 1 SEM). Ctrl 1 and Ctrl 2 correspond to endothelial cells incubated with CO2-independent medium or EGM-2 medium, respectively. Statistical analysis was performed using Student’s t test. *p < 0.05; **p < 0.01.
Fig 3: Endothelial injury and inflammatory markers in sepsis. A: The levels of ESM-1 decreased on day 7 after enrolment compared with day 1. B: The levels of HBP decreased on day 7 after enrolment compared with day 1. C: The levels of IL-6 decreased on day 7 after enrolment compared with day 1. D: The levels of TNF-α decreased on day 7 after enrolment compared with day 1. E: The levels of CD31 decreased on day 7 after enrollment compared with day 1.*P <0.05; †P <0.01; ‡P <0.001.ESM-1: Endothelial cell-specific molecule 1; HBP: Heparin-binding protein; IL-6: Interleukin 6; rhTPO: Recombinant human thrombopoietin; TNF-α: Tumor necrosis factor-α.
Fig 4: Conceptual schematic summarizing the proposed biological interplay between VEGF signaling, Endocan (ESM1), PDGF-CC/PDGF-DD signaling, and stromal activation, which may contribute to angiogenesis, microenvironment remodeling, treatment resistance, and outcomes in mCRC. Abbreviations: CAFs, cancer-associated fibroblasts; ECM, extracellular matrix; mCRC, metastatic colorectal cancer.
Fig 5: Comparison of serum Endocan, PDGF-DD, and PDGF-CC levels according to best response to chemotherapy, and their diagnostic performance in distinguishing non-responders. Optimal threshold values are indicated by circular markers on the ROC curves.
Supplier Page from Abcam for Human ESM1 ELISA Kit (Endocan)