Analysis of molecular responses in retinal ganglion cell death using RNAi

2014 Fiscal Year Final Research Report

• Project/Area Number: 25893015
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Ophthalmology
• Research Institution: Tohoku University
• Principal Investigator: FUJITA Kosuke 東北大学, 医学系研究科, 助手 (80708115)
• Project Period (FY): 2013-08-30 – 2015-03-31
• Keywords: Glaucoma / Adeno-associated virus / RNAi

Outline of Final Research Achievements

Glaucoma, a leading cause of blindness, is characterized by the progressive loss of retinal ganglion cells (RGCs); however, the molecular component modulated by cell death and the mechanisms of this modulation have not been fully understood.
Recently, our laboratory performed a comprehensive gene expression analysis of the murine retina in the optic nerve crush injury (Yasuda et al., 2014). To identify molecules involved in the RGS cell death signaling characterize their modulation, we conducted RNAi and overexpression experiments using adeno-associated virus. Using mice devoid of Chop and AAV2/2 carrying Chop transgene, we found that RGC death was indeed mediated specifically through Chop signaling, suggesting that ER stress seems to play an important role in the pathogenesis of RGC death following axonal injury, which is in agreement with recent comprehensive gene expression studies.

Free Research Field

分子生物学