Lipopolysaccharide Promotes Inflammatory Response via Enhancing IFIT1 Expression in Human Umbilical Vein Endothelial Cells.

Abstract

Atherosclerosis is an immune inflammatory disease and a major cause of mortality and morbidity worldwide. It is generally considered that a number of potent proinflammatory cytokines have a great influence on its pathogenesis, including IL-1β, IL-6, TNF-α, and NF-κB. A growing amount of empirical evidence indicates that the mechanism of cardiac dysfunction caused by lipopolysaccharide (LPS) is the activation of inflammation, but the exact mechanism in atherosclerosis is still unclear. Previous studies have shown that interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) participates in inflammation, but the effects and possible mechanism of action of IFIT1 on proinflammatory response remain largely unexplained. We found that LPS induced upregulation of IFIT1 expression in a time- and concentration-dependent manner in human umbilical vein endothelial cells (HUVECs). Overexpression of IFIT1 significantly upregulated LPS-induced expression of IL-1β, IL-6, TNF-α, and NF-κB in HUVECs. IFIT1-siRNA treatment dramatically decreased LPS-induced expression of IL-1β, IL-6, TNF-α, and NF-κB in HUVECs. The above results show that LPS induces expression of IL-1β, IL-6, TNF-α, and NF-κB through upregulating IFIT1 expression in HUVECs, and suggested that IFIT1 could act as potential therapeutic target to ameliorate atherosclerosis-related diseases.

• Authors: Jia-Li Wang, Fen Cai, Xue-Hui Liu, Li-Min Li, Xin He, Xiu-Mei Hu, Chun-Min Kang, Huan-Lan Bai, Ru-Yi Zhang, Chang-Meng Wu, Li-Mei Wu, Jia Wang, Lei Zheng, Bao-Hong Ping, Yan-Wei Hu, Qian Wang
• Journal: DNA and cell biology (DNA Cell Biol) Vol. 39 Issue 7 Pg. 1274-1281 (Jul 2020) ISSN: 1557-7430 [Electronic] United States
• PMID: 32551893 (Publication Type: Journal Article)

Chemical References

• Adaptor Proteins, Signal Transducing
• IFIT1 protein, human
• Lipopolysaccharides
• RNA-Binding Proteins

Topics

• Adaptor Proteins, Signal Transducing (genetics)
• Gene Expression Regulation (drug effects)
• Human Umbilical Vein Endothelial Cells (drug effects, metabolism)
• Humans
• Inflammation (chemically induced, genetics, metabolism)
• Lipopolysaccharides (pharmacology)
• RNA-Binding Proteins (genetics)