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

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K20247
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Ophthalmology
• Research Institution: Tohoku 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
• Keywords: 緑内障 / Ecel1

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.

Free Research Field

医歯薬学