| Project/Area Number |
15592024
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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 | Kagoshima University |
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Principal Investigator |
TOKUDA Masayuki Kagoshima University, University Hospital, Faculty of Medicine and Dentistry, Assistant Professor, 医学部・歯学部附属病院, 講師 (20253891)
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| Co-Investigator(Kenkyū-buntansha) |
TORII Mitsuo Kagoshima University, Graduate School of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (30116066)
NAGAOKA Shigetaka Kagoshima University, Graduate School of Medical and Dental Sciences, Associate Professor, 大学院・医歯学総合研究科, 助教授 (10155913)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2003: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Dental pulp cells / Temperature-sensitive receptor / VR-1 / Inflammatory cytokines / TNF-α / IL-6 / MAPK / apoptosis / TNF-a |
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| Research Abstract |
We examined whether human dental pulp fibroblasts(PF-10) have vanilloid receptor subtype 1(VR1) and its relationship with interleukin(IL)-6 expressions. Results of RT-PCR, Western blotting and immunocytochemical analysis indicate VR1 expression on PF-10 cells. As shown by ELISA, VR1 antagonist, capsazepine inhibited capsaicin-induced IL-6 production which is implicated in pulp inflammation. Furthermore, we investigated the activities of mitogen-activated protein kinases(MAPKs) in capsaicin induced IL-6 production. The phosphorylation of p38 MAPK and c-Jun NH_2-terminal kinase(JNK) were detected after capsaicin stimulation. p38 MAPK is involved in capsaicin-induced IL-6 production, as shown by the use of specific inhibitors of this kinase. The result of EMSA showed capsaicin inhibited tumor necrosis factor-alpha(TNF-α)-induced nuclear factor-kappa B(NF-κB) activations. These results suggest that the activation of VR1 may play an important role in dental pulp inflammation.
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