AAV2-mediated GRP78 Transfer Alleviates Retinal Neuronal Injury by Downregulating ER Stress and Tau Oligomer Formation
Author(s) -
Yonju Ha,
Wei Liu,
Hua Liu,
Shuang Zhu,
Fan Xia,
Julia E. Gerson,
Nisha A. Azhar,
Ronald G. Tilton,
Massoud Motamedi,
Rakez Kayed,
Wenbo Zhang
Publication year - 2018
Publication title -
investigative ophthalmology and visual science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.935
H-Index - 218
eISSN - 1552-5783
pISSN - 0146-0404
DOI - 10.1167/iovs.18-24427
Subject(s) - retinal ganglion cell , unfolded protein response , endoplasmic reticulum , optic nerve , programmed cell death , microbiology and biotechnology , chemistry , biology , neuroscience , biochemistry , apoptosis
Retinal ganglion cell (RGC) death following axonal injury occurring in traumatic optic neuropathy (TON) causes irreversible vision loss. GRP78 is a molecular chaperone that enhances protein folding and controls activation of endoplasmic reticulum (ER) stress pathways. This study determined whether adeno-associated virus (AAV)-mediated gene transfer of GRP78 protected RGCs from death in a mouse model of TON induced by optic nerve crush (ONC).
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