Identification of mechanisms underlying ectopic hyaloid invasion into retina in PHPV

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10898
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Ophthalmology
• Research Institution: Nagoya City University
• Principal Investigator: Yoshida Munenori 名古屋市立大学, 大学院医学研究科, 准教授 (60273447)
• Co-Investigator(Kenkyū-buntansha): 植村 明嘉 名古屋市立大学, 大学院医学研究科, 教授 (30373278) ; 小椋 祐一郎 名古屋市立大学, 大学院医学研究科, 教授 (70191963)
• Co-Investigator(Renkei-kenkyūsha): FUKUSHIMA Yoko 大阪大学, 医学系研究科, 助教 (70647031) ; NISHIYAMA Koichi 熊本大学, 国際先端医学研究機構, 准教授 (80398221)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: PHPV / 硝子体血管 / 網膜 / 内皮細胞 / Sema3E / PlexinD1 / RhoJ

Outline of Final Research Achievements

In persistent hyperplastic primary vitreous (PHPV), remaining hyaloid vessels often adhere to retinal surfaces. We previously found that in semaphorin 3E (Sema3E) knockout mice, hyaloid vessels ectopically invaded into retinas, leading to the formation of retinal folds (Fukushima et al. J Clin Invest 2011). In this research project, Sema3E derived from retinal ganglion cells bound to PlexinD1 on the endothelial cell surfaces of hyaloid vessels and activated a small GTPase RhoJ, thereby preventing ectopic hyaloid invasion into the retina.

Free Research Field

眼科学