Elucidation of the mechanism of suppression of outer nulear layer cell death of retinitis pigmentosa model rat retina by rapamycin.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10883
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Ophthalmology
• Research Institution: Chubu University
• Principal Investigator: NISHIZAWA Yuji 中部大学, 生命健康科学部, 教授 (80252229)
• Co-Investigator(Kenkyū-buntansha): 竹内 環 中部大学, 全学共通教育部, 助教 (90392018)
• Co-Investigator(Renkei-kenkyūsha): SAKAKIBARA Akira 中部大学, 生命健康科学部, 准教授 (20510217) ; HIRAKO Yoshiaki 名古屋大学, 大学院理学系研究科, 講師 (50377909) ; KONDO Mineo 三重大学, 大学院医学系研究科, 教授 (80303642)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 網膜色素変性症 / 網膜 / 視細胞 / ロドプシン / トランスジェニックラット / ラパマイシン / アポトーシス / オートファジー

Outline of Final Research Achievements

We successfully transiently suppressed visual photoreceptor death by microinjecting rapamycin to the eyeball of rhodopsin P347L transgenic rat (Tg rat), a retinal pigmentosa (RP) model rat. By rapamycin injection, mRNA expression levels of Bip and CHOP of the Tg rat retina were transiently and significantly decreased. On the other hand, mRNA expression level of Atg5 consistently increased significantly in Tg rats. Also, the fluorescence intensity of LC3 was greatly enhanced in visual cells after injection of rapamycin. From the above results, it was suggested that autophagy was transiently enhanced by injection of rapamycin into the Tg rat eyeball, and the ER stress response improved and apoptosis was delayed.

Free Research Field

網膜色素変性症の病態解析と治療の研究