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Glaucoma and oxidative stress

Research Project

Project/Area Number 24791882
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Ophthalmology
Research InstitutionUniversity of Occupational and Environmental Health, Japan

Principal Investigator

MIYAMOTO Naoya  産業医科大学, 医学部, 助教 (30620570)

Project Period (FY) 2012-04-01 – 2015-03-31
Project Status Completed (Fiscal Year 2014)
Budget Amount *help
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Keywords緑内障 / 酸化ストレス / 線維柱帯細胞 / 緑内障点眼薬 / 分子生物学 / 転写 / 線維柱帯
Outline of Final Research Achievements

Glaucomatous TM cells highly express sirt1 when compared with normal TM cells. Tafluprost induces the expression of sirt1 through the activation of the c-mic transcription factor. TM cells showed reduced sensitivity to H2O2 when cells were treated with tafluprost. In addition, both transcription factor c-myc and sirt1 expression was enhanced by drug induced signal transduction through its receptor.
These results indicate that tafluprost possesses a novel mechanism of action and function as potent protective agents against oxidative stress.

Report

(4 results)
  • 2014 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report
  • 2012 Research-status Report
  • Research Products

    (1 results)

All 2013

All Presentation (1 results)

  • [Presentation] タフルプロストは、c-myc/sirt1を活性化し、線維柱帯細胞を酸化ストレスから保護する。2013

    • Author(s)
      宮本直哉
    • Organizer
      日本眼科学会総会(117)
    • Place of Presentation
      東京国際フォーラム
    • Related Report
      2012 Research-status Report

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Published: 2013-05-31   Modified: 2019-07-29  

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