炎症
调节器
内皮细胞活化
细胞生物学
TLR4型
下调和上调
信号转导
内皮
生物
内皮干细胞
免疫学
癌症研究
医学
基因
内分泌学
体外
遗传学
作者
Jingjing Wang,Jingjing Fa,Pengyun Wang,Xinzhen Jia,Huixin Peng,Jing Chen,Yifan Wang,Chenhui Wang,Qiuyun Chen,Xin Tu,Qing Kenneth Wang,Chengqi Xu
标识
DOI:10.1016/j.cellsig.2017.04.011
摘要
Previous genetic studies suggested that variants in NINJ2 (encode ninjurin2) confer risk to ischemic stroke or large artery atherosclerotic stroke. However, the underlying mechanisms of NINJ2 in ischemic stroke or atherosclerosis are still unknown. In this study, we hypothesized that NINJ2 may play a role in endothelial inflammation and activation, and regulate the process of atherosclerosis. Here, we demonstrated that NINJ2 can regulate the expression of a panel of genes that are associated with inflammation and atherosclerosis (e.g. IL-1β, TNF-α, IL-8, IL-6, ICAM-1 and E-selectin) in human vascular endothelial cells (HUVECs). Moreover, we found the expression of ninjurin2 is upregulated in LPS stimulated HUVECs and mouse aorta, and it can regulate LPS-induced endothelial activation and the adhesion of monocytes to endothelial cells. We also found that NINJ2 can regulate NF-κB and c-jun through interacting with TLR4. In conclusion, our study suggests that ninjurin2 is a novel regulator of endothelia inflammation and activation through TLR4 signaling pathways, and these data provided new insights into the mechanisms between NINJ2 and atherosclerosis.
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