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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 ‐κB pathway
Author(s) -
Wan M.,
Liu J.,
Ouyang X.
Publication year - 2015
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12192
Subject(s) - nod1 , porphyromonas gingivalis , intercellular adhesion molecule 1 , cell adhesion molecule , cell adhesion , microbiology and biotechnology , nod , vcam 1 , downregulation and upregulation , biology , human umbilical vein endothelial cell , icam 1 , umbilical vein , chemistry , innate immune system , biochemistry , cell , receptor , nod2 , gene , genetics , bacteria , in vitro
Background and Objective Porphyromonas 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 ( NOD 1) 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 NOD 1 expression and the role that NOD 1 plays in the upregulation of VCAM ‐1 and ICAM ‐1. Material and Methods The 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‐κB 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). Results P. gingivalis invasion showed significant upregulation of NOD 1, VCAM ‐1 and ICAM ‐1. NOD 1 activation by meso‐diaminopimelic acid increased VCAM ‐1 and ICAM ‐1 expression, and NOD 1 gene silence reduced VCAM ‐1 and ICAM ‐1 release markedly. The NF ‐κB signaling pathway was activated by P. gingivalis , while NOD 1 gene silence decreased the activation of NF ‐κB. Moreover, inhibition of NF ‐κB reduced VCAM ‐1 and ICAM ‐1 expression induced by P. gingivalis in endothelial cells. Conclusion The results revealed that P. gingivalis induced NOD 1 overexpression in endothelial cells and that NOD 1 played an important role in the process of VCAM ‐1 and ICAM ‐1 expression in endothelial cells infected with P. gingivalis through the NF ‐κB signaling pathway.