| Project/Area Number |
11671885
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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 |
病態科学系歯学(含放射線系歯学)
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| Research Institution | Nihon University |
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Principal Investigator |
MATSUMOTO Hiroko Nihon University, Dentistry at Matsudo, Pharmacology, Research Assistant, 松戸歯学部, 助手 (50221594)
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| Co-Investigator(Kenkyū-buntansha) |
AKIMOTO Yoshiaki Nihon University, Dentistry at Matsudo, Oral Surgery 2, Associate Professor, 松戸歯学部, 助教授 (10147720)
FUJII Akira Nihon University, Dentistry at Matsudo, Pharmacology, Professor, 松戸歯学部, 教授 (70102564)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Calcium Channel Blocker / Nifedipine / protein phosphorylation / Human Gingival Fibroblast / Gingival Overgrowth / pHi / NSAID / [Ca^<2+>]i |
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| Research Abstract |
In order to clarify the mechanism of gingival overgrowth caused by calcium channel blockers, we have studied cellular responses in human gingival fibroblasts (hGFs) originated from nifedipine non-reactive patient (nifedipine non-responder, NIFn) and nifedipine reactive patient (nifedipine responder, NIFr).
1. Effect of nifedipine on protein phosphorylation
The present study was undertaken to identify the phosphorylated protein treated with bradykinin, thapsigargin, IL-1α, or nifedipine (NIF). NIF greatly stimulated the phospholylation specifically at 35 kDa protein in hGFs. The p38 phosphorylation caused by anisomycin was greater in NIFn than that of NIFr. Because of the capability of p38 inhibiting the cell cycle, it might be possible that cell proliferation of NIFr is greater than that of NIFn.
2. Effect of non-steroidal anti-inflammatory drugs (NSAIDs) on intracellular pH (pHi) and intracellular Ca^<2+> concentration ([Ca^<2+>]i)
We investigated the effects of stimulants (bradykinin, histamine, thapsigargin, cyclopiazonic acid) and NSAIDs on pHi in hGFs. All of stimulants and NSAIDs lowered pHi in hGFs and Tenidap and diclofenac Na greatly induced changes in pHi. Tenidap and mefenamic acid decreased the influx of extracellular [Ca^<2+>]i evoked by TG.These results indicate the possibility that Tenidap, diclofenac Na and mefenamic acid depress gingival overgrowth.
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