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The analysis of bone related diseases in cranio and oro-maxillofacial region by using A170 gene knockout mouse

Research Project

Project/Area Number 16591983
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Surgical dentistry
Research InstitutionUniversity of Tsukuba

Principal Investigator

YANAGAWA Toru  University of Tsukuba, Graduate school of comprehensive human sciences, assistant professor, 大学院人間総合科学研究科, 講師 (10312852)

Co-Investigator(Kenkyū-buntansha) ISHII Tetsuro  University of Tsukuba, Graduate school of comprehensive human sciences, professor, 大学院人間総合科学研究科, 教授 (20111370)
Project Period (FY) 2004 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
KeywordsA170 / sequestosome / Paget's disease of bone / Nrf2 / peroxiredoxin I / Paget骨病
Research Abstract

The purpose of this study is to elucidate the role of A170 gene, which is causative gene of Paget's disease of bone, in the bone related diseases in cranio-oro-maxillofacial region by using A170 gene knockout mouse.
At first, we repeated backcross of knockout mice because the value of bone morphometry was not constant. While backcross was undergoing, we analyzed the phenotype of Nrf2 knockout mouse, because Nrf2 was transcription factor of oxidative stress inducible proteins and Nrf2deficient mouse lacks A170 induction. Since Peroxiredoxin I was regulated by Nrf2, we measured the elimination capacity of reactive oxygen species in Peroxiredoxin I deficient mouse to prepare estimation of oxidative stress in A170 knockout mouse.
After backcross was repeated, we performed bone morphometry. The parameters of bone morphometry : osteoid surface, osteoid thickness, eoroded surface, osteoclast surface, trabecular number, mineral apposition rate, and bone formation rate were significantly different between knockout mouse and wild type mouse. The osteoblast from calvaria of mouse embryo was cultured, and alkaline phosphatase activity and Arizarin Red-S staining density were measured. There was tendency that the osteoblastic activity was lower in the knockout mice. The other phenotypes of A170 gene knockout mouse were hyperphagia, obesity, and insulin resistance. Insulin resistance was proved by-glucose and insulin loaded test. Glucose uptake was proved to be reduced by using isotope labeled 2-deoxyglucose. From those results osteoblastic function was damaged in A170 knockout mouse and insulin signal may be associated with this phenomenon.

Report

(4 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • 2004 Annual Research Report
  • Research Products

    (8 results)

All 2006 2005 2004

All Journal Article (8 results)

  • [Journal Article] Tissue Prx I in the protection against Fe-NTA and the reduction of nitroxyl radicals2006

    • Author(s)
      Junya Uwayama
    • Journal Title

      Biochem Biophys Res Commun 339(1)

      Pages: 226-231

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Tissue Prx I in the protection against Fe-NTA and the reduction of nitroxyl radicals2006

    • Author(s)
      Junya Uwayama, et al.
    • Journal Title

      Biochem Biophys Res Commun 339(1)

      Pages: 226-231

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Tissue Prx I in the protection against Fe-NTA and the reduction of nitroxyl radicals2006

    • Author(s)
      Junya Uwayama et al.
    • Journal Title

      Biochem Biophys Res Commun 339(1)

      Pages: 226-231

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Protective role of Nrf2 in disease including oral disease2005

    • Author(s)
      Toru Yanagawa
    • Journal Title

      J Oral Biosci 47(2)

      Pages: 126-134

    • NAID

      110003166663

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary 2005 Annual Research Report
  • [Journal Article] Protective role of Nrf2 in disease including oral disease2005

    • Author(s)
      Toru Yanagawa, et al.
    • Journal Title

      J Oral Biosci 47(2)

      Pages: 126-34

    • NAID

      110003166663

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Nrf2 deficiency causes tooth decolourization due to iron transport disorder in enamel organ2004

    • Author(s)
      Toru Yanagawa
    • Journal Title

      Genes to Cells 9(7)

      Pages: 641-651

    • NAID

      120007131624

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Nrf2 deficiency causes tooth decolorization due to iron transport disorder in enamel organ2004

    • Author(s)
      Toru Yanagawa, et al.
    • Journal Title

      Genes to Cells 9(7)

      Pages: 641-651

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Nrt2 deficiency causes tooth decolourization due to iron transport disorder in enamel organ2004

    • Author(s)
      Toru Yanagawa
    • Journal Title

      Genes to Cells 9(7)

      Pages: 641-651

    • Related Report
      2004 Annual Research Report

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Published: 2004-04-01   Modified: 2016-04-21  

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