Porphyromonas gingivalis, Periodontal pathogen, lipopolysaccharide induces angiogenesisvia extracellular signal-regulated kinase 1/2 activation in human vascular endothelial cells

2007 ◽  
Vol 30 (1) ◽  
pp. 34-42 ◽  
Author(s):  
Tae Hyeon Koo ◽  
Hyung Oh Jun ◽  
Soo-Kyung Bae ◽  
Su-Ryun Kim ◽  
Chang-Pyo Moon ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Porphyromonas Gingivalis ◽  
Vascular Endothelial Cells ◽  
Periodontal Pathogen ◽  
Vascular Endothelial ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal

scholarly journals Invasion of Human Vascular Endothelial Cells byActinobacillus actinomycetemcomitans via the Receptor for Platelet-Activating Factor

2000 ◽  
Vol 68 (9) ◽  
pp. 5416-5419 ◽  
Author(s):  
Harvey A. Schenkein ◽  
Suzanne E. Barbour ◽  
C. R. Berry ◽  
Barbara Kipps ◽  
John G. Tew
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Platelet Activating Factor ◽  
Systemic Circulation ◽  
Oral Bacteria ◽  
Periodontal Pathogen ◽  
Vascular Endothelial ◽  
Transmission Electron ◽  
Paf Receptor ◽  
Paf Receptor Antagonist

ABSTRACT Strains of the periodontal pathogen Actinobacillus actinomycetemcomitans are variable with respect to display of phosphorylcholine (PC)-bearing antigens. We have examined strains ofA. actinomycetemcomitans with and without PC to assess their ability to invade endothelial cells via the receptor for platelet-activating factor (PAF). Results of antibiotic protection assays indicate that PC-bearing A. actinomycetemcomitansinvade human vascular endothelial cells by a mechanism inhibitable by CV3988, a PAF receptor antagonist, and by PAF itself. The invasive phenotype was verified by transmission electron microscopy. A PC-deficient strain of this organism was not invasive. This property, in addition to the established ability of A. actinomycetemcomitans to invade epithelial cells, may provide this organism with access to the systemic circulation. The ability of PC-bearing oral bacteria to access the circulation may also explain the elevated levels of anti-PC antibody in serum found in patients with periodontitis.

scholarly journals Mechanism of temporal gradients in shear-induced ERK1/2 activation and proliferation in endothelial cells

2001 ◽  
Vol 281 (1) ◽  
pp. H22-H29 ◽  
Author(s):  
Xuping Bao ◽  
Chuanyi Lu ◽  
John A. Frangos
Keyword(s):  
Endothelial Cells ◽  
Intracellular Signaling ◽  
Proliferative Response ◽  
Vascular Endothelial Cells ◽  
Inhibitory Effect ◽  
Steady Shear ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Extracellular Signal ◽  
Intracellular Signaling Cascade

The aim of the current study was to investigate the intracellular signaling cascade that leads to temporal gradients in shear (TGS)-induced endothelial cell proliferation, with a focus on the involvement of extracellular signal-regulated kinases 1 and 2 (ERK1/2). With the use of well-defined pulsatile, impulse, step, and ramp laminar flow profiles, we found that TGS (impulse flow and pulsatile flow) induced an enhanced and sustained (>30 min) phosphorylation of ERK1/2 relative to step flow (which contains a step increase in shear followed by steady shear), whereas steady shear (ramp flow) alone downregulated activated ERK1/2. Nitric oxide (NO) was found to mediate both the stimulatory effect of TGS and the inhibitory effect of steady shear on endothelial ERK1/2 phosphorylation. Reactive oxygen species (ROS) were also demonstrated to be associated with TGS-induced ERK1/2 phosphorylation. Both Gq/11 and Gi3 were necessary for the activation of ERK1/2 by TGS. Finally, the TGS-induced endothelial proliferative response was abolished by ERK1/2 inhibition. Our study demonstrated the essential role of G proteins, NO, and ROS in TGS-dependent ERK1/2 activation and proliferative response in vascular endothelial cells.

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