ArticleInvestigative ophthalmology & visual science2018
AAV2-mediated GRP78 Transfer Alleviates Retinal Neuronal Injury by Downregulating ER Stress and Tau Oligomer Formation.
Article in Investigative ophthalmology & visual science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- GRP78 in human diseases: From molecular chaperone to therapeutic target.Theranostics · 2026Review
- CXCR3 Deficiency Alleviates Retinal Ganglion Cell Loss by Regulating Neuron-Astrocyte Communication in a Mouse Model of Glaucoma.Investigative ophthalmology & visual science · 2025Article
- Glucose-Regulated Protein 78, via Releasing β-Catenin from Adherens Junctions, Facilitates Its Interaction with STAT3 in Mediating Retinal Neovascularization.The American journal of pathology · 2024Article
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- Sirt6 protects retinal ganglion cells and optic nerve from degeneration during aging and glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Cytokine Levels in Experimental Branch Retinal Vein Occlusion Treated With Either Bevacizumab or Triamcinolone Acetonide.Translational vision science & technology · 2024Article
- Inhibition of TLR4/NF-κB pathway and endoplasmic reticulum stress by overexpressed S100A4 ameliorates retinal ischemia-reperfusion injury of mice.Molecular neurobiology · 2024Article
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Keratin8 Deficiency Aggravates Retinal Ganglion Cell Damage Under Acute Ocular Hypertension.Investigative ophthalmology & visual science · 2023Article
- Acacetin antagonized lipotoxicity in pancreatic β-cells via ameliorating oxidative stress and endoplasmic reticulum stress.Molecular biology reports · 2022Article
- mTORC1 regulates high levels of protein synthesis in retinal ganglion cells of adult mice.The Journal of biological chemistry · 2022Article
- Targeting Endoplasmic Reticulum Stress as an Effective Treatment for Alcoholic Pancreatitis.Biomedicines · 2022Review
- Endoplasmic reticulum stress: New insights into the pathogenesis and treatment of retinal degenerative diseases.Progress in retinal and eye research · 2020Review
- Multiple Herpes Simplex Virus-1 (HSV-1) Reactivations Induce Protein Oxidative Damage in Mouse Brain: Novel Mechanisms for Alzheimer's Disease Progression.Microorganisms · 2020Article
- Neuronal Epac1 mediates retinal neurodegeneration in mouse models of ocular hypertension.The Journal of experimental medicine · 2020Article
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- Neuroprotective Effects of HSF1 in Retinal Ischemia-Reperfusion Injury.Investigative ophthalmology & visual science · 2019Article
- DDIT3 (CHOP) contributes to retinal ganglion cell somal loss but not axonal degeneration in DBA/2J mice.Cell death discovery · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Purpose: 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). Methods: ONC was induced by a transient crush of optic nerve behind the eye globe. AAV was used to deliver genes into retina. Molecules in the ER stress branches, tau oligomers, and RGC injury were determined by immunohistochemistry or Western blot. Results: Among tested AAV serotypes, AAV2 was the most efficient for delivering genes to RGCs. Intravitreal delivery of AAV2-GRP78 markedly attenuated ER stress and RGC death 3 days after ONC, and significantly improved RGC survival and function 7 days after ONC. Protein aggregation is increased during ER stress and aggregated proteins such as tau oligomers are key players in neurodegenerative diseases. AAV2-GRP78 alleviated ONC-induced increases in tau phosphorylation and oligomerization. Furthermore, tau oligomers directly induced RGC death, and blocking tau oligomers with tau oligomer monoclonal antibody (TOMA) attenuated ONC-induced RGC loss. Conclusion: These data indicate that the beneficial effect of AAV2-GRP78 is partially mediated by the reduction of misfolded tau, and provide compelling evidence that gene therapy with AAV2-GRP78 or immunotherapy with TOMA offers novel therapeutic approaches to alleviate RGC loss in TON.
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Registered trials
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