| Project/Area Number |
16591846
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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 |
Morphological basic dentistry
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| Research Institution | Tsurumi University |
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Principal Investigator |
INOUE Hiroko Tsurumi University, School of Dental Medicine, Assistant Professor, 歯学部, 講師 (50367306)
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| Co-Investigator(Kenkyū-buntansha) |
MISHIMA Kenji Tsurumi University, School of Dental Medicine, Associate Professor, 歯学部, 助教授 (50275343)
YAMADA Koichi Tsurumi University, School of Dental Medicine, Research Associate, 歯学部, 助手 (60367307)
TSUBOTA Kazuo Keio University, School of Medicine, Professor, 医学部, 教授 (40163878)
SAITO Ichiro Tsurumi University, School of Dental Medicine, Professor, 歯学部, 教授 (60147634)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Estrogen / Endocrine disruptor / Epstein-Barr virus / エストロジェン / EBウィルス |
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| Research Abstract |
To study the possibility of EBY reactivation by estrogen and endocrine disruptors, we analyzed BZLF1 promoter assay and immunoblotting for ZEBRA protein. Estradiol inhibited ZEBRA expression induced by TPA in B95-8 and Akata cells. We established stable B95-8 cell lines which transfected pZp221-Luc and pZp552-Luc. In these cells estradiol also inhibited luciferase activity activated by TPA. In Hela, HSY and HSG cells, estradiol inhibited Zp activity induced by both ZEBRA transfection or TPA stimulation. The effect of estrogen was revealed in 30 minutes, thus we speculated a part of these effects might be a non-genomic event through membrane ER or GPR30. The mechanisms of estrogen on Zp activity are being searched in detail. Next, we analyzed the effects of endocrine disruptors with the same procedure using BPA,3-MC,B[a]P and TCDD. None of these chemicals changed the ZEBRA expression or Zp activity in B94-8 and Akata cells. In contrast to these effects on B cells, Zp activity was enhanced by 3-MC and TCDD in Hela, HSG and HSY cells. When we transfected AhR/Arnt and ER, the activity of Zp was decreased in Hela cells whereas enhanced in HSG and HSY cells compared with AhR/Arnt alone. These results indicated that ER could regulate the Zp activity induced by dioxins depending on the cell types. In HSY cells, although ZEBRA transactivation of Zp was not changed by dioxins without AhR/Arnt, high activity of Zp was observed when ZEBRA and AhR/Arnt were cotransfected. We speculated that dioxins might be an enhancer of EBV reactivation in epithelial cells. To determine the interaction between AhR/Arnt and ZEBRA, we are investigating using immunoprecipitation, GST pull-down assay, Gel shift assay and foot printing.
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