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2018 Fiscal Year Final Research Report

Role of transcription factor Sp1 in retinal ganglion cell death in mouse glaucoma model animals

Research Project

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Project/Area Number 17K16956
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Ophthalmology
Research InstitutionTohoku University

Principal Investigator

Tsuda Satoru  東北大学, 大学病院, 助教 (60791093)

Project Period (FY) 2017-04-01 – 2019-03-31
Keywords網膜神経保護 / 緑内障 / 外傷性視神経症 / Sp-1 / Ecel1 / 視神経挫滅
Outline of Final Research Achievements

When Ecel1 expression was evaluated in the mouse retina after optic nerve crush, focusing on Ecel1 downstream of Sp-1, Ecel1 expression was specifically induced in retinal ganglion cells. In addition, knocking down the Ecel1 gene using the Adeno-Associated Virus-CRISPR / Cas9 system and evaluating retinal ganglion cell survival with retrograde labeling, qRT-PCR, and visual evoked potentials, knockdown of Ecel1 promoted the loss of retinal ganglion cells after optic nerve crush. This results indicate that Ecel1 may be a novel therapeutic target for alleviation of retinal ganglion cell injury. And it is speculated that Ecel1 is involved in a part of cytoprotective mechanism of Sp-1.

Free Research Field

緑内障

Academic Significance and Societal Importance of the Research Achievements

本研究において明らかにされた、転写因子であるSp-1の下流にあるEcel1による視神経挫滅後の網膜神経節細胞障害の軽減効果は、視神経が障害され、重篤な視機能障害を来す緑内障や外傷性視神経症に対して、Sp-1及びEcel1が新規治療標的となりえることを示している。緑内障は、本邦の失明原因の第1位の疾患であり、既存治療である眼圧下降治療が十分に奏功せず失明に至る症例が存在する。また外傷性視神経症は有効な治療法が存在しない。そのため本研究成果は、緑内障や外傷性視神経症による重篤な視機能障害や失明の防止に繋がる可能性のある有意義な研究成果と考えられる。

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Published: 2020-03-30  

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