The roles of Alarmin for the pathophysiology of Atopic Retinal Detachment

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670738
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Ophthalmology
• Research Institution: Juntendo University
• Principal Investigator: KAWANO Hiroyuki 順天堂大学, 医学部, 准教授 (70234094)
• Co-Investigator(Kenkyū-buntansha): MATSUDA Akira 順天堂大学, 大学院医学研究科, 准教授 (00312348) ; EBIHARA Nobuyuki 順天堂大学, 医学部, 教授 (20255699) ; MORI Kazuhiko 京都府立医科大学, 大学院医学研究科, 講師 (50327805)
• Co-Investigator(Renkei-kenkyūsha): NAKAE Susumu 東京大学, 医科学研究所, 准教授 (60450409) ; TADA Nobuhiro 順天堂大学, 大学院医学研究科, 准教授 (50338315)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: アトピー / 網膜剥離 / アラーミン

Outline of Final Research Achievements

To elucidate roles 'Alarmins', which released from the injured tissue to alert danger to the neighbor healthy tissue, for the pathophysiological process of atopic retinal detachment, we investigated mouse retinal detachment models made by perforating retinal injury. We found positive immunolocalization of interleukin-33 (IL-33), a prototype of the alarmin, in the nuclei of the Muller glial cells of the healthy mouse retina. Upon perforating retinal injury, IL-33 released from the nuclei to the vitreo-retinal interface, and upregulate profibrotic genes in the injured retina. The results suggested that IL-33 may be a good therapeutic target or atopic retinal detachment in future.

Free Research Field

眼科学