期刊
CELLULAR SIGNALLING
卷 35, 期 -, 页码 231-241出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2017.04.011
关键词
NINJ2; Atherosclerosis; Endothelial; Inflammation; TLR4
类别
资金
- National Natural Science Foundation of China Program [31671302, 31430047, 81600263, 81200073]
- Natural Science Foundation of Hubei Province [2016CFB224]
- Fundamental Research Funds for the Central Universities [HUST0118170142]
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-1 beta), TNF-alpha, 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-kappa B 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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