Associations between periodontal infection and cardiovascular disease have been documented. Porphyromonas gingivalis is a well-established periodontal pathogen, and tissue factor (TF) is a key initiator of the coagulation cascade. In this context, P. gingivalis has been reported to enhance TF expression in human endothelial cells. The present study investigated the underlying mechanisms of TF induction by P. gingivalis in human umbilical vein endothelial cells. P. gingivalis increased TF expression in a dose- and time-dependent manner. Not only live bacteria but also glutaraldehyde-fixed bacteria increased TF expression to the same extent. However, sonicates of P. gingivalis did not induce TF expression. Cytochalasin D and SMIFH2, which are inhibitors of actin polymerization and actin nucleation, respectively, inhibited the TF expression induced by P. gingivalis . Finally, TF production was decreased or increased in the presence of various signaling inhibitors, including mitogen-activated protein kinases. These results suggest that P. gingivalis induces endothelial TF expression by a bacterial internalization-dependent mechanism and through diverse signal transduction mechanisms.

Introduction
Materials and Methods
    1. Reagents
    2. Bacterial culture
    3. Cell culture
    4. Reverse transcription-polymerase chain reaction(RT-PCR)
    5. Enzyme-linked immunosorbent assay (ELISA)
    6. Statistical analysis
Results
    1. Dose- and time-dependent TF induction byP. gingivalis
    2. Comparison between live, killed, and sonicatedP. gingivalis
    3. Effects of CD and SMIFH2 on the induction of TFand MCP-1 by P. gingivalis
    4. Effects of various signaling inhibitors on theproduction of TF by P. gingivalis
Discussion
References

• Vu Phuong Dong(Department of Pharmacology and Dental Therapeutic, College of Dentistry, Chosun University)
• Hoon Yoo(Department of Pharmacology and Dental Therapeutic, College of Dentistry, Chosun University) Correspondence to