Involvement of excess neuropeptide by axon reflex in idiopathic pulpitis
| Project/Area Number |
22592125
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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 |
OYAMA Tohru 鹿児島大学, 大学院・医歯学総合研究科, 助教 (60233623)
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| Research Collaborator |
MIYASHITA Keiko 鹿児島大学, 医学部・歯学部附属病院, 助教 (50636264)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 特発性歯髄炎 / 軸索反射 / 神経ペプチド / 神経原生炎症 / アナンダマイド / マトリックスメタロプロテアーゼ / 神経原性炎症 |
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| Research Abstract |
In this study, AEA (Anandamide), CGRP (Calcitonin gene-related peptide), VIP (Vasoactive intestinal peptide) and SubstanceP induced MMP-2 production in HPC (human cells dental pulp cells) in culture. HPC expressed all 3 types of AEA receptor (CB1, CB2, and TRPV-1). AEA-induced MMP-2 production was blocked by CB1 or TRPV-1 antagonists and by small interfering RNA for CB1 or TRPV-1. Furthermore, c-jun N-termialkinase inhibitor also reduced MMP-2 production. We demonstrated for the first time that AEA induced MMP-2 production via CB1 and TRPV-1 in HPC.
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Report
(4 results)
Research Products
(4 results)
