ArticleInvestigative ophthalmology & visual science2013
Excitotoxicity upregulates SARM1 protein expression and promotes Wallerian-like degeneration of retinal ganglion cells and their axons.
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- Intravitreal injection of SARM1 siRNA in TNF-induced optic nerve degeneration.International ophthalmology · 2025Article
- SARM1: The Checkpoint of Axonal Degeneration in the Nervous System Disorders.Molecular neurobiology · 2025Review
- Downregulation of SARM1 Protects Retinal Ganglion Cell Axonal and Somal Degeneration Via JNK Activation in a Glaucomatous Model of Ocular Hypertension.Investigative ophthalmology & visual science · 2024Article
- Programmed axon death: a promising target for treating retinal and optic nerve disorders.Eye (London, England) · 2024Review
- Loss of Sarm1 reduces retinal ganglion cell loss in chronic glaucoma.Acta neuropathologica communications · 2024Article
- Role of Nuclear NADAdvances in experimental medicine and biology · 2023Review
- SARM1 Ablation Is Protective and Preserves Spatial Vision in an In Vivo Mouse Model of Retinal Ganglion Cell Degeneration.International journal of molecular sciences · 2022Article
- An inducible rodent glaucoma model that exhibits gradual sustained increase in intraocular pressure with distinct inner retina and optic nerve inflammation.Scientific reports · 2021Article
- Article
- Neuroprotection in Glaucoma: NADCells · 2021Review
- TDP-43 mislocalization drives neurofilament changes in a novel model of TDP-43 proteinopathy.Disease models & mechanisms · 2021Article
- SARM1 deficiency promotes rod and cone photoreceptor cell survival in a model of retinal degeneration.Life science alliance · 2020Article
- Destructive Effect of Intravitreal Heat Shock Protein 27 Application on Retinal Ganglion Cells and Neurofilament.International journal of molecular sciences · 2020Article
- Wallerian degeneration as a therapeutic target in traumatic brain injury.Current opinion in neurology · 2019Review
- Axon injury signaling and compartmentalized injury response in glaucoma.Progress in retinal and eye research · 2019Review
- Schwann cells shape the neuro-immune environs and control cancer progression.Cancer immunology, immunotherapy : CII · 2019Review
- Prospects of siRNA cocktails as tools for modifying multiple gene targets in the injured spinal cord.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- Restoring retinal neurovascular health via substance P.Experimental cell research · 2019Article
- Pathological classification of equine recurrent laryngeal neuropathy.Journal of veterinary internal medicine · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeThis study investigated the role of sterile alpha/Armadillo/Toll-Interleukin receptor homology domain 1 protein (SARM1) in Wallerian-like degeneration of retinal ganglion cells (RGCs) and their axons after inducing excitotoxicity.
methodsTo induce excitotoxicity, kainic acid (KA) was injected into the vitreous humor of B6.Cg-Tg(Thy1-YFP)HJrs/J mice. Control mice received PBS. At 24, 48, and 72 hours after injection, degeneration of RGCs and their axons in the retina was determined by fundus imaging, and axonal degeneration in the optic nerves was determined by fluorescence microscopy. SARM1 protein levels were determined by Western blot analysis and SARM1 tissue localization was determined by immunohistochemistry. Causal role of SARM1 in KA-mediated degeneration of RGCs and their axons was determined by treating the eyes with KA along with Sarm1 silencer siRNA.
resultsFundus imaging and microscopic analysis indicated that KA promoted Wallerian-like degeneration of RGCs and axons in KA-treated eyes, but not in PBS-treated eyes. Quantitative analysis indicated a significant increase in degeneration of RGCs and their axons in KA-treated injected eyes, but not in PBS-treated eyes. Compared with low levels of SARM1 protein in retinal protein extracts, retinal cross sections, and optic nerve from PBS-treated eyes, SARM1 protein levels were increased in KA-treated eyes. Finally, treatment of eyes with KA along with a Sarm1 silencer siRNA attenuated KA-mediated degeneration of RGCs and their axons significantly.
conclusionsResults presented in this study, for the first time, show that KA-mediated upregulation of SARM1 protein promotes Wallerian-like degeneration of RGCs and their axons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.