Interleukin-27 Enhances TNF-α-mediated Upregulation of Inflammatory Cytokine and Chemokine / 现代生物医学进展

Objective:Immune cells and inflammatory mediators play important roles in the development of atherosclerotic vascular inflammation.This study focuses on the direct effect ofIL-27 on human coronary artery endothelial cells.Methods:In this study,the effects of IL-27 and TNF-α on inflammatory cytokines and chemokines were investigated.Results:IL-27 could significantly enhance the TNF-α-mediated upregulation of inflammatory cytokine IL-6 and chemokines CCL5 from human coronary artery endothelial cells.The release of IL-6 and CCL5 was significantly suppressed by specific signaling molecule inhibitors.Conclusion:The induction of these mediators from the human coronary artery endothelial cells could be differentially regulated by the c-Jun N-terminal kinase,p38 mitogen-activated protein kinase,and nuclear factor-κB pathways.These results provided new insights into the effect of IL-27 on the TNF-α mediated activation of human coronary artery endothelial cells in atherosclerotic vascular inflammation.

Effect of sphingosine-1-phosphate receptor 2 on coronary endothelial cells proliferation / 实用医学杂志

Objective To explore the role of sphingosine-1-phosphate receptor (S1PR2) in human coronary artery endothelial cell proliferation in vitro. Methods MTT assay was used to detect cell proliferation in human coronary artery endothelial after treatment of S1P and S1PR2 antagonist JTE-013. Phosphor-ERK and total- ERK level were measured by western blot in endothelial after treatment of S1P and JTE-013. Results 1 μmol/L S1P significantly increased endothelial cells proliferation. S1PR2 antagonist JTE-013 inhibited S1P-induced endothelial cell proliferation in dose-dependent manner. S1PR2 antagonist JTE-013 significantly inhibited S1P-induced phosphor-ERK level in endothelial cells. Conclusion S1PR2 may involve in S1P-induced endothelial cell proliferation through activation of ERK pathway.