Porphyromonas gingivalis induces vascular cells expression of Egr-1 and Cyr61 in atherosclerosis
Date Issued
2009
Date
2009
Author(s)
Wang, Hsi-Wen
Abstract
According to the 2007 census of department of health, Executive Yuan, ROC, heart disease and cerebral vascular disease rank second and third among ten leading causes of death, respectively. Epidemiological studies have shown that periodontal disease is associated with increased risk for cardiovascular and cerebrovascular disease. With Porphyromonas gingivalis (P.g.) as the most important periodontal pathogen, this organism can accelerate atheroma deposition in animal models. However, the detail mechanism remains unknown. Previous studies have shown that Cyr61 and Egr-1 are highly expressed in human atherosclerotic plaques, correlating with the degree of stenosis and plaque histopathology. Inhibition of Cyr61 and Egr-1 gene expression reduces neointimal hyperplasia following balloon injury in rats. Here we show 1μg/ml P. g. LPS markedly induces Cyr61 and Egr-1 in mRNA and protein level in human vascular smooth muscle cell (VSMC) and human monocytic THP-1 cells. Pretreatment with NF-kB inhibitor Bay 11-7082, ERK inhibitor PD98059, JNK inhibitor SP600125, p38 MAPK inhibitor SB203580 and antioxidant epigallocatechin gallate (EGCG) significantly reduced P. g. LPS-induced Cyr61 in human vascular smooth muscle cells (VSMC), whereas the induction of Egr-1 via P. g. LPS only affected by SP600125 and curcumin (AP-1 inhibitor). In THP-1 cells, pretreatment with ROS inhibitor NAC, Bay 11-7082, PD98059, SP600125 and EGCG significantly reduced P. g. LPS-induced Cyr61, but not SB203580. The induction of Egr-1 by P. g. LPS in THP-1 also affected by SP600125 and curcumin. In conclusion, our results provide the first evidence that chronic P.g. infection may contribute to atherogenesis through sustained upregulation of Cyr61 and Egr-1.
Subjects
atherosclerosis
SDGs
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