2004 Fiscal Year Final Research Report Summary
The role and expression mechanism of an inflammatory mediator in human denial pulp cell
| Project/Area Number |
15592034
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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 |
Conservative dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
HASHIZUME Hideki Nihon University, School of Dentistry at Matsudo, Lecturer(Full-Time), 松戸歯学部, 講師 (10256894)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUSHIMA Kiyoshi Nihon University, School of Dentistry at Matsudo, Professor, 松戸歯学部, 教授 (00157306)
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| Project Period (FY) |
2003 – 2004
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| Keywords | human dental pulp cell / Plasminogen activator / IL-1β / protein tyrosin kinase |
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| Research Abstract |
1.IL-1β(50pg/ml) activated t-PA in the lysate and medium in a time-dependent (0〜12hrs) manner.
2.IL-1β activated t-PA in the lysate and medium in a concentration -dependent(50〜100pg) manner.
3.Pyrrolidine dithocarbamate, a NFκB inhibitor inhibited the IL-1β-induced tPA activation.
4.Genistein and herbimycin, protein tyrosine kinase inhibitors, inhibited the IL-1β-induced tPA activation.
5.On the contrary, orthovanadate, a protein tyrosine phosphatase inhibitor, augmented the effect of IL-1β.
These observations suggest that regulation of tyrosine phosphorylation is necessary for IL-1β induced t-PA activation, and the synthesis of t-PA via NFκB is involved in the effect of IL-1β in HDP.
6.Phorbol 12-myrisatate 13-acetate, protein kinase C activator t PA augmented the effect if IL-1β induced tPA activation.
7.Ionomycine, Ca^<2+> mobilizing reagent did not augment the IL-1β induced tPA activation
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