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Nucleotide-binding oligomerization domain 1 regulates Porphyromonas gingivalis-induced vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 expression in endothelial cells through NF-kappa B pathway
Wan, M.1; Liu, J.1; Ouyang, X.1,2
关键词Endothelial Cell Intercellular Adhesion Molecule-1 Nucleotide-binding Oligomerization Domain 1 Vascular Cell Adhesion Molecule 1
刊名JOURNAL OF PERIODONTAL RESEARCH
2015-04-01
DOI10.1111/jre.12192
50期:2页:189-196
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Dentistry, Oral Surgery & Medicine
研究领域[WOS]Dentistry, Oral Surgery & Medicine
关键词[WOS]P38 MAPK ; ACTIVATION ; INFLAMMATION ; RECEPTORS ; NOD1 ; RECOGNITION ; DISEASE
英文摘要

Background and ObjectivePorphyromonas gingivalis has been shown to actively invade endothelial cells and induce vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) overexpression. Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular pattern recognition reporter, and its involvement in this process was unknown. This study focused on endothelial cells infected with P.gingivalis, the detection of NOD1 expression and the role that NOD1 plays in the upregulation of VCAM-1 and ICAM-1.

Material and MethodsThe human umbilical vein endothelial cell line (ECV-304) was intruded by P.gingivalis W83, and cells without any treatment were the control group. Expression levels of NOD1, VCAM-1, ICAM-1, phosphorylated P65 between cells with and without treatment on both mRNA and protein levels were compared. Then we examined whether mesodiaminopimelic acid (NOD1 agonist) could increase VCAM-1 and ICAM-1 expression, meanwhile, NOD1 gene silence by RNA interference could reduce VCAM-1, ICAM-1 and phosphorylated P65 release. At last, we examined whether inhibition of NF-B by Bay117082 could reduce VCAM-1 and ICAM- 1 expression. The mRNA levels were measured by real-time polymerase chain reaction, and protein levels by western blot or electrophoretic mobility shift assays (for phosphorylated P65).

ResultsP.gingivalis invasion showed significant upregulation of NOD1, VCAM-1 and ICAM-1. NOD1 activation by meso-diaminopimelic acid increased VCAM-1 and ICAM-1 expression, and NOD1 gene silence reduced VCAM-1 and ICAM-1 release markedly. The NF-B signaling pathway was activated by P.gingivalis, while NOD1 gene silence decreased the activation of NF-B. Moreover, inhibition of NF-B reduced VCAM-1 and ICAM-1 expression induced by P.gingivalis in endothelial cells.

ConclusionThe results revealed that P.gingivalis induced NOD1 overexpression in endothelial cells and that NOD1 played an important role in the process of VCAM-1 and ICAM-1 expression in endothelial cells infected with P.gingivalis through the NF-B signaling pathway.

语种英语
WOS记录号WOS:000350914600006
项目编号81070840
资助机构National Natural Science Foundation of China
引用统计
被引频次:13[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52895
专题北京大学口腔医学院_牙周科
作者单位1.Natl Engn Lab Digital & Mat Technol Stomatol, Beijing, Peoples R China
2.Peking Univ, Sch & Hosp Stomatol, Dept Periodontol, Beijing 100081, Peoples R China
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Wan, M.,Liu, J.,Ouyang, X.. Nucleotide-binding oligomerization domain 1 regulates Porphyromonas gingivalis-induced vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 expression in endothelial cells through NF-kappa B pathway[J]. JOURNAL OF PERIODONTAL RESEARCH,2015,50(2):189-196.
APA Wan, M.,Liu, J.,&Ouyang, X..(2015).Nucleotide-binding oligomerization domain 1 regulates Porphyromonas gingivalis-induced vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 expression in endothelial cells through NF-kappa B pathway.JOURNAL OF PERIODONTAL RESEARCH,50(2),189-196.
MLA Wan, M.,et al."Nucleotide-binding oligomerization domain 1 regulates Porphyromonas gingivalis-induced vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 expression in endothelial cells through NF-kappa B pathway".JOURNAL OF PERIODONTAL RESEARCH 50.2(2015):189-196.
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