The Influence of Porphyromonas gingivalis Groel in Vascular Cells

Project: A - Government Institutionb - National Science and Technology Council

Project Details


Previous reports demonstrated that the high proportion of atherosclerosis sufferer hold the antibodies of Porphyromonas gingivalis (P. gingivalis) in their plasma. Recent studies showed that large amount of GroEL accumulate in P. gingivalis-infected vessel wall, which may accelerate the atherogenesis. In in vitro study, infection of P. gingivalis induced IL-6 expression in endothelial cells. In animal study, P. gingivalis induced proliferation of vascular smooth muscle cells, accumulation of macrophages under sub-endothelial space, and severe the atherogenesis. Although more evidences demonstrated that GroEL of P. gingivalis may induce atherosclerosis, the underlying mechanisms remain to be elucidated. Thrombomodulin is a kind of protein which regulates blood coagulation. Vascular endothelial cells express thrombomodulin which is a receptor of thrombin. Thrombomodulin is associated with the occurrence of deep vein thrombosis, cardiovascular diseases, carcinogenesis, and embryogenesis. The investigation on animal model demonstrated that thrombomodulin may reduce the arterial intimal hyperplesia, inhibit the infiltration of leukocytes, and restrain the proliferation and migration of smooth muscle cells in balloon-injuryed rabbits. Overexpressed of thrombomodulin may inhibit the expression of adhesion molecules in vascular cells. Whether GroEL of P. gingivalis influence thrombomodulin expression in vascular cells, and the underlying mechanisms remain to be elucidated. Post balloon angioplasty restenosis is the problem that the clinical medical science often meets up, but the balloon angioplasty is one of the main methods that cure the coronary arteries disease. Therefore, concentrate on machine of understanding these afferent diseases' turning and guard against the work, is an urgent research. Take place restenosis machine turns to sophisticate very. Previous studies demonstrated that chronic infection is also one of the factors that cause the restenosis and atherosclerosis. The Gram-negative bacteria will through the toll-like receptor (TLR4) inducing inflammation although the lipopolysaccharide not inducing the immune response. Increasing of TLR4 expression will raise the cells sensitivity to lipopolysaccharide, accelerate the atherogenesis. Frantz S. et al. demonstrated that the cardiomyocytes express the TLR4 constitutively, and TLR4 will increase greatly in cardiomyopathy, this result was corroborated in animal experiments; In vitro, endothelial and smooth muscle cells express the TLR4, and will increase by pro-inflammatory factors stimulation, and caused the downstream inflammation responses; Kristina E. demonstrated that atherosclerotic plaque express TLR4, these performances were relationship with inflammatory signaling pathway. However, whether GroEL of P. gingivalis influence TLR4 expression in vascular smooth muscle cells which resulting in vascular restenosis after PTCA remain unclear. This study will employ cell biology and molecular biology to investigate the influence of P. gingivalis GroEL on thrombomodulin change in endothelial cells and TLR4 expression in vascular smooth muscle cells; futuremore, the mouse femoral artery cuff-injury model and Rabbit abdominal aorta endolectomy model will be used. We expect that the results of present study will provide insights into the development of therapeutic strategies for the prevention of atherosclerosis and restenosis.
Effective start/end date8/1/147/31/15


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