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Vascular endothelial cells play an important role in leukocyte traffickingduring the inflammatory process. Proinflammatory cytokines activate the expressionof cell adhesion molecules in endothelial cells. Janus kinase (JAK) and signaltransducer and activator of transcription (STAT) are important intracellular cytokinesignaling molecules that are involved in immune responses. The purpose of thisstudy was to investigate the effect of JAK3 inhibition on the expression of tumornecrosis factor (TNF)-α-induced cell adhesion molecules in vascular endothelialcells and to evaluate the therapeutic potential of JAK3 for myocardial vascularpermeability in endotoxemic mice. A JAK3 inhibitor, JANEX-1, decreased the TNF-α-inducedexpression of intercellular adhesion molecule (ICAM)-1, VCAM (vascular cell adhesionmolecule)-1 and fractalkine in human umbilical vein endothelial cells (HUVECs).The downregulation of the expression of these cell adhesion molecules by JANEX-1was mediated via suppression of STAT3 phosphorylation and nuclear factor-κB (NF-κB)activation. In endotoxemic mice, pretreatment with JANEX-1 prevented not onlyan increase in the cardiac ICAM-1 expression by LPS in the arteriolar and capillaryendothelial cells, but also myocardial vascular leakage. These results suggestthat inhibition of the JAK/STAT pathway by JANEX-1 ameliorates the expressionof TNF-α-induced cell adhesion molecules in HUVECs and improves myocardial vascularpermeability.

international journal of molecular medicine

Janex-1, a JAK3 inhibitor, ameliorates tumor necrosis factor‑α‑induced expression of cell adhesion molecules and improves myocardial vascular permeability in endotoxemic mice