ApoM Suppresses TNF-α-Induced Expression of ICAM-1 and VCAM-1 Through Inhibiting the Activity of NF-κB

被引:22
|
作者
Gao, Ji-Juan [1 ]
Hu, Yan-Wei [1 ]
Wang, Yan-Chao [1 ]
Sha, Yan-Hua [1 ]
Ma, Xin [2 ]
Li, Shu-Fen [1 ]
Zhao, Jia-Yi [1 ]
Lu, Jing-Bo [3 ]
Huang, Chuan [1 ]
Zhao, Jing-Jing [1 ]
Zheng, Lei [1 ]
Wang, Qian [1 ]
机构
[1] Southern Med Univ, Nanfang Hosp, Lab Med Ctr, Guangzhou 510515, Guangdong, Peoples R China
[2] Southern Med Univ, Nanfang Hosp, Dept Anesthesiol, Guangzhou 510515, Guangdong, Peoples R China
[3] Southern Med Univ, Nanfang Hosp, Dept Vasc Surg, Guangzhou 510515, Guangdong, Peoples R China
关键词
CELL-ADHESION MOLECULE-1; TUMOR-NECROSIS-FACTOR; APOLIPOPROTEIN-M; VASCULAR INFLAMMATION; ACTIVATION; PHOSPHORYLATION; PROTEIN; ATHEROSCLEROSIS; NF-KAPPA-B1; METABOLISM;
D O I
10.1089/dna.2015.2892
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To explore the anti-inflammatory effect of apolipoprotein M (apoM) on regulation of tumor necrosis factor- (TNF-)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and further investigate the molecular mechanism of apoM in this process. We found that TNF- could decrease expression of apoM and inhibitor of NF-B- (IB) in HepG2 cells. Overexpression of apoM caused a significant decrease of ICAM-1 and VCAM-1 expression, while it caused a significant increase of IB expression in HepG2 cells. Furthermore, the treatment with TNF- could increase ICAM-1 and VCAM-1 expression, decrease IB protein expression, and increase nuclear factor-B (NF-B) activity, and these effects were markedly enhanced by small interfering RNA (siRNA)-mediated silencing of apoM in HepG2 cells. Our findings demonstrated that apoM suppressed TNF--induced expression of ICAM-1 and VCAM-1 through inhibiting the activity of NF-kappa B.
引用
收藏
页码:550 / 556
页数:7
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