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Functional analysis of Ecel 1 in animal model of glaucoma and its application to therapy

Research Project

Project/Area Number 15K20247
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Ophthalmology
Research InstitutionTohoku University

Principal Investigator

Sato Kota  東北大学, 医学系研究科, 助教 (50732327)

Project Period (FY) 2015-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Keywords緑内障 / Ecel1 / 神経保護
Outline of Final Research Achievements

In this study, we aimed at the mechanism of expression and functional analysis of Ecel 1, which is expressed in the retina of glaucoma model mice. From the results of qPCR, western blotting and immunostaining, when retinal ganglion cell damage was induced by optic nerve crush, Ecel 1 was highly expressed in retinal ganglion cells 4 days after optic nerve crush. Although Ecel 1 is not induced by oxidative stress or NMDA injury, it is highly expressed by dysfunction of axonal transport as well as optic nerve crush. In order to analyze the function of Ecel1 in the retina, we made AAV2-mEcel1 virus vector which highly expresses Ecel1 in retinal ganglion cell. when this virus was administered in the eyes and optic nerve crush was carried out, unlike the hypothesis, no neuroprotective effect was observed in the group expressing high Ecel 1.

Report

(3 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • Research Products

    (1 results)

All 2015

All Presentation (1 results)

  • [Presentation] マウス視神経挫滅モデルの網膜神経節細胞障害におけるECEL1の関与2015

    • Author(s)
      志賀由己浩
    • Organizer
      第26回日本緑内障学会
    • Place of Presentation
      ういんくあいち(愛知県)
    • Year and Date
      2015-09-11
    • Related Report
      2015 Research-status Report

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Published: 2015-04-16   Modified: 2021-01-27  

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