| Project/Area Number |
17591991
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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 | Okayama University |
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Principal Investigator |
ARAI Hideo Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Associate Professor, 大学院医歯薬学総合研究科, 助教授 (70222718)
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| Co-Investigator(Kenkyū-buntansha) |
TAKASHIBA Shogo Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Professor, 大学院医歯薬学総合研究科, 教授 (50226768)
NISHIMURA Fusanori Hiroshima University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Professor, 大学院医歯薬学総合研究科, 教授 (80208222)
NARUISHI Koji Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Assistant Professor, 大学院医歯薬学総合研究科, 助手 (00346446)
TANIMOTO Ichiro Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Assistant Professor, 大学院医歯薬学総合研究科, 助手 (00280686)
MAEDA Hiroshi Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Senior Assistant Professor, 医学部・歯学部附属病院, 講師 (00274001)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | dentin-pulp complex / rat wounded pulp / TNF-α signaling / promoter activity / transcription factor-binding site / over-expression / cell death / TNF-αパスウェイ |
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| Research Abstract |
Pulpal wound healing followed by cavity preparation may involve reactionary or reparative dentinogenesis in relation to the cavity position; however, little is known about the molecular responses. We aimed to isolate and analyze genes induced or suppressed in the wounded pulp to identify molecular processes involved in the pulp responses to injury. Twenty-three cDNAs were isolated by cDNA subtraction between healthy and wounded pulp of rats. By library screening, we identified rat 14.7K-interacting protein (rFIP)-2A and B genes homologous to human FIP-2, being involved in regulating membrane trafficking and cellular morphogenesis. RT-PCR analysis showed induction for only rFIP-2B in the wounded pulp. In situ hybridization analysis revealed unique expression of rFIP-2s in adult and embryonic tissues of rats. Transcription of rFIP-2A and B was regulated by alternative use of promoters at rFIP-2 locus. When the rFIP-2A or B-pAcGFP1-Golgi construct was transfected into normal rat kidney (NRK-52E) cells, rFIP-2B was localized in Golgi of whereas rFIP-2A, which is a truncated protein lacking the N-terminal 250 amino acids of rFIP-2B, existed ubiquitously in the cytoplasm. In rat pulp fibroblasts (RPC-C2A) cells, rFIP-2B was significantly induced by tumor necrosis factor (TNF)-α, and the induction was dependent on c-jun N-terminal kinase (JNK) pathway. rFIP-2B was localized in the cytoplasm, and translocated into the nucleus by cell death stimuli. The results suggest that rFIP-2 expression is regulated by the alternative promoter site, and rFIP-2B is a crucial molecule mediated by TNF-a, may be involved in cell death pathway during pulp inflammation.
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