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. 2021 Dec 10;22(24):13288. doi: 10.3390/ijms222413288

Figure 1.

Figure 1

The effects of IL-33 on human ECs. The release of IL-33 occurs following severe tissue damage upon cell injury, necrosis, mechanical stress or infection. When released, IL-33 binds to ST2 receptor on the cell surface as well as to circulating sST2, which negatively regulates IL-33-signalling. Upon binding to ST2 receptor, IL-33 activates several intracellular pathways, including the NF-κB-pathway. It was previously shown that IL-33 induces inflammatory activation of ECs and increases endothelial expression of IL-1, IL-6, IL-8, VCAM-1, ICAM-1, E-selectin and MCP-1. Evidence indicates that IL-33 also increases the expression and activity of u-PA, PAI-1 and TF in human ECs via ST2/NF-κB-pathway. In addition, mRNA and protein expressions of TFPI are reduced. At the same time, IL-33 induces the release of procoagulant MVs from ECs, but the mechanism for this effect remains unclear. In this manner, IL-33 activates human endothelium and promotes a proinflammatory, angiogenic and thrombotic state of human ECs. IL: interleukin; VCAM-1: vascular cell adhesion molecule-1; ICAM-1: intercellular adhesion molecule-1; E-selectin: endothelial selectin; MCP-1: monocyte chemoattractant protein-1; u-PA: urokinase-type plasminogen activator; PAI-1: plasminogen activator inhibitor type-1; TF: tissue factor; TFPI: tissue factor pathway inhibitor; MVs: microvesicles. Upwards arrows indicate upregulation, downwards arrows indicate downregulation.