| Project/Area Number |
12672009
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
矯正・小児・社会系歯学
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| Research Institution | Health Sciences University of Hokkaido |
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Principal Investigator |
HIROSE Kimiharu Health Sciences University of Hokkaido, School of Dentistry, Associate Professor, 歯学部, 助教授 (10218836)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Porphyronmonas gingivalis / Fimbriae / Endothelium / Adhesion / Trypsin / Heart disease / 歯周病原性細菌 / 歯周病 / レセプター |
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| Research Abstract |
To Investigate extrinsic blood coagulation pathway, factor VII must be activated to VIIa. Trypsin is known to activate factor VII to VIIa. Here I show that Porphyromonas gingivalis fimbriae stimulate trypsinogen mRNA expression and its protein production in human coronary artery endothelial cells (HCAEC) culture. The monolayer of HCAEC were incubated with or with out various doses of the fimbriae. RT-PCR and western blot analysis were perfomed ti detect and analyze trypsinogen expression in HCAEC. The fimbriae stimulated the expression of trypsinogen mRNA and production of its protein in a fimbriae dose dependent manner. The fimbriae binding to HACEC was specifically evidenced by a binding assay involving radio labeled fimbriae. Additionally, anti-fimbriae antibody (EF3-11) inhibited the fombriae-induces expression of trypsinogen in HCAEC. Finally, inductive effect of trypsinogen production by the fimbriae in HCAEC were inhibited by H7 an inhibitor of PKC. These results demonstrated that fimbriae bind HCAEC, which subsequently lead to stimukate of abnormal blood coagulation factor. These results thus suggest that the possible roles of the periodontopathesic bacteria in abnormal blood coagulation in human heart vascular system.
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